In the face of varying marketing messages, shopping for a probiotic can be overwhelming. Some companies champion products with high CFU (colony-forming units, which is the measurement of groups of living microorganisms observed under the microscope), while others showcase products with dozens of strains. With more product options than ever, it is important to know what to look for when selecting a probiotic.
So what is a probiotic?
Scientists define a probiotic as the following: “Live microorganisms that, when administered in adequate amounts, confer a health benefit on the host.”1,2
Based on that definition, how do you find the probiotic you need? Here is a checklist of six things to look for:
Personalization—What health benefits do you need?
Science—Clinically studied to demonstrate health benefits
Identity—Genus, species, and strain
Amounts matter—Billions are not always better
Alive through expiration
Manufacturing quality/testing for contaminants and purity
Submitted by the Metagenics Marketing Team
"I'm addicted to sugar"
We’ve all heard or thought this before. Considering the American palate for highly processed, overly sweetened foods and the ubiquitous nature of sugar in advertising, we see evidence of a concerning shift. Sugar’s role in the American diet has moved beyond a character actor and into a starring role. Further, as discussed in the previous post, Sugar. How Much Is Too Much?, we consume far more sugar than is recommended for our health. But the question remains—are we addicted?
More please: How sugar affects the brain
While an ICD-10 code for “sugar addiction,” has yet to be established, an increasing body of research tells us that sugar has addictive effects on the brain.1,2 Like sex and drugs, consuming sugar stimulates the release of dopamine, a neurotransmitter that gives us a sense of euphoria and controls the reward and pleasure centers in the brain. But what may have evolved as a survival mechanism has gone rogue.
The caveman sweet tooth
From an anthropological perspective, we are hard-wired for sweetness. The pleasing taste of sweet foods was a conditioned reward, one which could increase early man’s survival odds. In times of food scarcity, a preference for more nutritionally dense foods might have provided the energy required to continue the hunt, outrun a predator, or simply avoid starvation.
Flash forward a few hundred thousand years, and sugar is exponentially more abundant. Consistent intake of concentrated sugar can lead to changes in the brain’s dopamine receptors. Similar to increased drug or alcohol tolerance, over time, more sugar is needed for the same “high.”
Cookies and cocaine
So, the more you eat, the more you want. But, as for being “addictive” animal studies have shown sugar consumption to have drug-like effects. These include sugar-related bingeing, craving, tolerance, and withdrawal. In fact, according to a Connecticut College study, Oreo cookies cause more neural activation in the brains of rats than cocaine.3
For many individuals, the only way to stop over-consuming sugar is to stop the cravings. But the only way to end the cravings is to stop feeding them with sugar. So, in addition to cutting out the obvious forms of sugar—candy, baked goods, etc.—it is important to be aware of the less obvious forms of sugar in your diet. Over the course of a day, small quantities can add up, keep your cravings alive, and thwart your efforts to take control of sugar. So become a sugar sleuth. Here are five tips to get you started.
5 Tips for Identifying Added Sugars
The journey to a healthy relationship with sugar starts with awareness. Watch for the next post in this series, which will feature strategies for taking control of sugar.
You eat when you’re hungry. When you’re full, you put down your fork.
It sounds simple, right? Not always.
Some of us succumb to cravings even when we’re satiated. In fact, chances are that most of us have experienced cravings at one time or another. A recent study indicated 97% of women and 68% of men report feeling cravings at one time or another.1
But what are cravings? Why do we crave certain foods more than others? And, from a physiological standpoint, how does satiety work? This post will go over the details.
What is satiety?
Satiety is what we experience after eating a meal or snack. Normal satiety involves not only feeling full after sufficient intake, but also experiencing the need to limit consumption until the next time we get hungry.2
The brain is closely linked to satiety. The central nervous system—and more specifically, the hypothalamus—is responsible for letting us know when we’re ready to stop eating.2
Here are some of the factors that can affect the way we regulate our food intake:2
There are other factors that might occur as well.2 For instance, our physical activity levels and the pleasure we experience from eating can also affect satiety.3
And while most people stop eating when they’re satiated, others may continue to indulge long after the body signals it’s full.2 This is where food cravings come in.
What causes cravings?
Just as the brain affects satiety, it also plays an important role in food cravings.3,4
Cravings are the products of signals from the brain regions responsible for pleasure, memory, and rewards. These regions include the hippocampus, insula, and caudate. In many cases, the brain regions responsible for memory—those that associate specific foods with pleasure—are especially active when we crave fatty, sugary, or salty foods.4,5
There are a number of other factors that have also been linked to cravings:
Before we move on, it’s worth noting that cravings can be either selective or nonselective in nature. Selective cravings are for specific foods, like a greasy burger or a slice of rich chocolate cake.4
These types of cravings could also be specific for sugar, salt, or fat.4 If you find yourself lingering in the candy aisle, reaching for that pint of ice cream you keep in the freezer, and pouring yourself cup after cup of your favorite sweetened coffee drink, you likely have a selective craving for sugar.
Non-selective cravings, conversely, don’t target specific foods. Instead, they represent a desire to eat or drink anything—and they could be the result of real hunger or thirst. If you notice these types of cravings, drink plenty of water and make sure you’re getting enough to eat. By doing so, you may be able to address these non-selective cravings relatively quickly.4,5
What are some strategies for overcoming cravings?While there’s no harm in succumbing to the occasional craving, we should all strive to adopt a nutritious diet. We’ll be healthier and happier, and the brain and body will thank us for eating nutrient-dense foods.1,3-5
With that, here are some tips for overcoming unhealthy food cravings:
So socialize with a friend. Take a hike in nature. Sit down with a good book. Do what you can to relax and find joy in your life and not on your plate.
We can replace our cravings with healthier alternatives.4 For example, instead of reaching for a sugar-laden, fruit-flavored carton of yogurt, opt for the plain alternative and sweeten it yourself—in moderation—with fresh fruit, all-natural honey, or pure maple syrup.
So try not to let yourself get too hungry—and focus on nutritious foods. Eating more protein, healthful fats, colorful produce, and whole grains throughout the day will keep your hunger in check without triggering a potential craving.3-5
While these strategies can help us manage our cravings, they aren’t our only options. Again, it’s essential to drink enough water throughout the day.4 And we can always step away from the fridge the next time a craving hits, and engage in a non-food-related, pleasure-inducing activity instead. We might stretch our muscles, spend time with family, or listen to music. Contacting your healthcare practitioner to discuss cravings and changes to diet may also be a good idea.
For more information on nutrition and general wellness topics, please visit the Metagenics blog.
by Ashley Jordan Ferira, PhD, RDN
Recent research from three well-known cohorts, The Nurses’ Health Study (NHS), NHS2 and Health Professionals’ Follow-Up Study (HPFS), reveals that higher magnesium intake is associated with lower risk of type 2 diabetes (T2D), particularly in diets with poor carbohydrate quality.1
Green leafy vegetables, unrefined whole grains, and nuts are richest in magnesium, while meats and milk contain a moderate amount.2 Refined foods, like carbohydrates (carb), are poor sources of magnesium. Diets with poor carb quality are characterized by higher glycemic index (GI), higher glycemic load (GL), and lower fiber intake. These poor carbs require a higher insulin demand.
The typical American diet is low in vegetables and whole grains, resulting in reduced magnesium intake. The Recommended Daily Allowance (RDA) for magnesium is 310-320 mg/day for adult women and 400-420 mg/day for adult men.3 Half of the US population fails to meet their daily magnesium needs, and hypomagnesemia exists in 1/3 of adults.4-5 Magnesium is needed for normal insulin signaling; current research has linked insufficient magnesium intake to prediabetes, insulin resistance and T2D.4 Increased magnesium intake has been inversely associated with T2D risk in observational studies.6
Collaborators from Tufts University, Harvard University, and Brigham and Women’s Hospital, sought to investigate the impact of magnesium intake, from both dietary and supplemental sources, on the risk of developing T2D in subjects who had diets with poor carb quality and raised GI, GL, or low fiber intake.1 They followed three large prospective cohorts, NHS, NHS2 and HPFS (totaling over 202,700 participants). Dietary intake was quantified by validated food frequency questionnaires (FFQ) every 4 years, and T2D cases were captured via questionnaires. Over 28 years of follow-up, there were 17,130 cases of T2D.
Major study findings included:1
Similar to the US population estimates, 40-50% of study participants had inadequate magnesium intake. A healthful, varied diet and supplemental magnesium (especially in diets that restrict or exclude carbohydrates, dairy or meat) are essential to ensure sufficient daily magnesium intake.
Why is this Clinically Relevant?
Link to Abstract
by Bianca Garilli, ND
Magnesium is the 4th most abundant mineral in the human body following calcium, sodium, and potassium. Intracellularly, magnesium is the 2nd most abundant cation behind only potassium.1 The number of essential roles magnesium plays in the body is extraordinary, with over 300 enzymes requiring magnesium as a co-factor for proper functioning.1
This essential element is involved in numerous critical physiological processes such as energy production (ATP metabolism, oxidative phosphorylation, and glycolysis), protein synthesis, muscle contraction, nerve function, blood glucose control, hormone receptor binding, blood pressure regulation, trans membrane ion flux, gating of calcium channels, cardiac excitability, and synthesis of nucleic acids (RNA and DNA).1
Unfortunately, magnesium is one of the most prevalent nutrient gaps in the US. The 2015 Dietary Guidelines Advisory Committee noted a substandard intake of magnesium as compared to the Estimated Average Requirement (EAR), which is the Dietary Reference Intake (DRI) used to assess population sufficiency vs. insufficiency for nutrients.2-3 A 2016 publication in Advanced Nutrition concluded, “Approximately 50% of Americans consume less than the EAR for magnesium, and some age groups consume substantially less”.4 This is especially concerning when one considers the critical implications of long-term, frequently unrecognized magnesium deficiencies.
Deficiencies in magnesium can present with overt clinical manifestations such as nausea, vomiting, lethargy, weakness, personality changes, tetany and tremor, seizures, arrhythmia, and muscle fasciculations.5 In other cases, sub clinical deficiencies may be more difficult to recognize yet have equally serious effects if left untreated. Health concerns and disease processes resulting from an underlying, subclinical magnesium deficiency may contribute to low bone mineral density and cardio-metabolic implications such as metabolic syndrome, hypertension, arrhythmia, arterial calcification, atherosclerosis, heart failure, and increased risk for thrombosis.6
A sub clinical magnesium deficiency can also disrupt sleep and cause muscle cramping, two common symptoms often glossed over but which can be signs of a bigger problem if left untreated. The impact of magnesium on these two clinical manifestations will be explored further:
Magnesium and sleep
A double-blind randomized clinical trial composed of 43 elderly participants between 60-75 years of age with diagnosed insomnia was conducted.7 The experimental group was given 500 mg/day of elemental magnesium for 8 weeks (250 mg elemental magnesium from 414 mg of Mg oxide, twice daily), while the control group received a placebo for the same length of time.7 A statistically significant increase was seen in sleep time, sleep efficiency, and concentration of serum renin and melatonin, as well as a significant decrease in insomnia severity index (ISI) score, sleep onset latency, and serum cortisol level.7
For many individuals, sleep is disrupted by restless leg syndrome (RLS) or periodic limb movements (PLMS).8 A study supplementing 12.4mmol of oral magnesium in the evenings for 4-6 weeks found that the overall sleep efficiency improved from 75 to 85%.9 The Mg-supplemented group also experienced a significant reduction in PLMS associated with arousal (7 PLMS/hr vs. 17 PLMS/hr at baseline).9
Magnesium and muscle cramps
Muscle cramping is a common occurrence among women during pregnancy, in athletes, and in the elderly, for which magnesium is often recommended.10 There are only a few studies, however, that have reviewed the efficacy of magnesium for muscle cramping.10 In a Cochrane review, 7 trials (5 parallel, 2 cross-over design) were included, with 3 of these trials studying pregnancy-associated leg cramps in 202 females and 4 trials looking at idiopathic leg cramps in 322 participants.10 Results from the studies noted no significant improvement of muscle cramping in older adults, while results in pregnancy were mixed leading the authors to recommend further studies in this population.10 The authors of a review article in Scientifica note that the mixed findings may be explained by the potential that, “deficiencies of other elemental nutrients including calcium and potassium have also been implicated in muscle cramps and spasms. It may be that magnesium is potentially helpful in situations of magnesium deficiency but is not of use if the problem is related to deficiency of another nutrient.”1
Magnesium: Daily needs and sources
Magnesium is an essential macro-mineral required by the human body. The prevalence of deficiency from serum measurements ranges from 12.5-20% of the population.11 Due to the necessity of this cation for over 300 reactions in the human body and the high risk of deficiency, magnesium levels should be routinely monitored either through blood testing and/or a diet diary review. If found to be low, magnesium stores can be replaced through increasing daily intake of the mineral through nutrition as well as routine supplementation.
Foods groups high in magnesium content include green leafy vegetables, legumes, nuts, seeds, and whole grains.12 Specific foods with high magnesium levels include spinach, Swiss chard, beet greens, turnip greens, pumpkin seeds, summer squash, soybeans, sesame seeds, quinoa, black beans, cashews, sunflower seeds, brown rice and pinto beans.12
The Recommended Dietary Allowance (RDA) for magnesium varies by age, sex, and whether pregnant or lactating:13
*RDA not able to be determined; Adequate Intake (AI) reported
Supplementation with high-quality magnesium is another, targeted way to reach optimal levels and fill dietary gaps. Supplementation dosing and form can be personalized and taken orally via capsules, tablets, liquid, and even powder. Some of the different forms available in the market include Mg oxide, gluconate, chloride, citrate, sulfate, glycinate, and L-threonate.
Bianca Garilli, ND
Dr. Garilli is a former US Marine turned Naturopathic Doctor (ND). She works in private practice in Northern California as well as running a consulting company working with leaders in the natural and functional medicine world such as the Institute for Functional Medicine and Metagenics. She is passionate about optimizing health and wellness in individuals, families, companies and communities- one lifestyle change at a time. Dr. Garilli has been on staff at the University of California Irvine, Susan Samueli Center for Integrative Medicine and is faculty at Hawthorn University. She is the creator of the Veterans for Health Initiative and is the current President of the Children’s Heart Foundation, CA Chapter.
At grocery stores across America, more and more people are choosing to buy organic produce. Why? The answer is simple: pesticides. Tests conducted by the US Department of Agriculture showed nearly 70 percent of 48 conventionally grown produce samples to be contaminated with pesticides. Even more frightening is the total of 178 different pesticides found on the thousands of products sampled by the USDA—often present even after the produce was washed.1
Although higher prices may deter you from buying organic, there’s even more frightening information about conventionally grown fruits and vegetables that may change your mind.
Your Choices Matter
A 2015 study found that people who mostly or exclusively buy organic foods had a significantly lower level of pesticides in their urine samples—in spite of the fact that they eat 70 percent more servings of fruits and veggies every day compared to adults who rarely (or never) buy organic.2 And according to several long-term studies, the dangers of pesticides appear to be amplified for children whose brain and nervous system development may be impaired by prolonged exposure.3-5 The fact is, your everyday choices really do make a difference!
The Dirty Dozen
It may seem overwhelming to make the organic switch, but due to the amount of research available on pesticide contamination, it doesn’t have to be. There are 12 specific foods you should always purchase organic whenever possible, a.k.a. the Dirty Dozen:
Because more than 90 percent of samples tested positive for the presence of at least one pesticide, these foods have been singled out for containing the highest amounts of pesticide residue. Look for the USDA sticker whenever you shop for these to help you avoid exposure.
The Clean Fifteen
Buying organic may not always be attainable. Fortunately, there’s also a group of foods called the “Clean Fifteen,” which make the cut for containing a relatively low concentration of pesticide residue:
Some of these foods, when tested, contained no pesticides whatsoever! If you can’t always buy organic, these are the safest kinds of conventional produce—for both your health and your budget.
Take Care of You
Eating organic produce is well worth it when you consider the downside to conventionally grown produce that is, more often than not, completely contaminated with harmful pesticides. By choosing organic when you buy anything off the Dirty Dozen list, you’ll make a small change that can lead to monumental improvements in your health.
For more information and access to both annual lists, visit the Environmental Working Group website.
Submitted by the Metagenics Marketing Team
What we know for clinical practice and decision making
by Sara Gottfried, MD, and Kari Hamrick, PhD, RD
Polycystic ovary syndrome (PCOS) is a problem of hormone dysregulation that can lead to irregular menstrual cycles, high androgens, and its downstream sequelae such as acne and hirsutism, infertility, weight gain, and cardiovascular disease. As practitioners and their affected female patients anguish over the root cause and solutions, one part is very clear: up to 85% of women with PCOS are insufficient in vitamin D.1 For our patients with PCOS, correcting low serum vitamin D levels can be a helpful lever in improving hormonal, metabolic, inflammatory, and possibly cardiovascular outcomes.
Vitamin D is known as the “sunshine vitamin” because sunlight can trigger cutaneous synthesis of vitamin D. Previously, I reviewed the role of vitamin D in the body and the prevalence of vitamin D deficiency and insufficiency across populations. Vitamin D is a steroid hormone precursor that has hundreds of roles in the body beyond bone health. Having been interested in vitamin D deficiency and the connection with health issues, especially those impacting women, I wanted to delve into the link between vitamin D and PCOS. I will review the current literature to help inform clinical practice and decision making for this unique patient group.
PCOS and women’s health
PCOS is the most common endocrine disorder among women during reproductive years, with an estimated prevalence of 4-18% from puberty to perimenopause.2,3 Prevalence varies based on ethnicity (i.e., in descending order: Black > Middle Eastern > Caucasian > Chinese).4 Clinical presentation may include insulin resistance, obesity, hirsutism (excess male pattern hair growth), and chronic low-grade inflammation.5,6 PCOS has been linked to serious health concerns, including increased risk of breast and endometrial cancers, infertility, heart disease, stroke, dysglycemia, insulin resistance, gestational diabetes, and preeclampsia.5,6
Women experiencing hormonal imbalance at any age may feel out of control and even disempowered. Women seeking help for PCOS deserve compassionate healthcare providers who are able to diagnose, understand the root causes of their symptoms, and provide evidence-based guidelines for measurable and effective health improvement.
Recently updated international PCOS guidelines have made diagnosis and care for patients more comprehensive, standardized, and evidence-based.7 In the summer of 2018, an international consortium of PCOS healthcare professionals, including 37 societies across 71 countries (spanning six continents), issued a guideline for the assessment and management of PCOS, with 31 evidence-based recommendations that help refine the therapeutic approach and increased the focus on the important role of education and lifestyle modification.7
I understand the desire to employ best practices with the most available research evidence in your clinic. But with patients coming and going all day, it is easy to become overwhelmed with journals piling up on your desk and not enough time in the day to do a targeted PubMed search, much less read all of the new hits. Along with key individuals clinical studies, the aforementioned international consensus guideline,7 as well as systematic reviews and meta-analyses, are a time-efficient way to help the clinician recognize patterns and synthesize evidence to identify answers or solutions to important research and clinical questions.8 Now, let’s explore the vitamin D-PCOS link further, from epidemiologic to intervention evidence.
THE VITAMIN D-PCOS LINK
Vitamin D status and PCOS
Systematic review of vitamin D research indicates that hypovitaminosis D (low serum 25-hydroxvitamin D [25(OH)D]) is common in women with PCOS.9 In a review of PCOS etiology, average serum 25(OH)D levels ranged 11–31 ng/mL, but the majority of patients (67%–85%) had values < 20 ng/mL,1 which is the cutoff for deficiency according to a vitamin D clinical practice guideline from the US Endocrine Society.10
Serum vitamin D status is inversely associated with PCOS symptoms and pathology, including obesity,11,12cardiovascular disease risk,13 and insulin resistance.2,11 In a clinical study investigating the impact of lifestyle intervention on health outcomes in women with overweight or obesity and PCOS, higher 25(OH)D concentrations were significantly associated with lower waist circumference and total cholesterol among participants of both cohorts.14
Taken together, these findings suggest that vitamin D status is an important therapeutic consideration for women with PCOS.
Vitamin D supplementation and PCOS
Vitamin D supplementation studies show promising results for the potential impact of this essential micronutrient in PCOS symptomology. A 2018 systematic review and meta-analysis examined 11 randomized controlled trials (RCTs) including > 600 patients with PCOS; as expected, vitamin D deficiency and insufficiency were observed to be prevalent in this patient group, and vitamin D supplementation significantly improved 25(OH)D status.15 Analyses considered factors like dose frequency and whether vitamin D supplementation was provided alone or as a co-supplement. Major findings include: continuous daily supplementation (i.e., as opposed to weekly bolus dosing) with vitamin D (< 4,000 IU/day) alone reduced homeostatic model assessment of insulin resistance (HOMA-IR). Vitamin D provided as a co-supplement (i.e., in combination with other micronutrients – vitamin K, calcium, zinc, or magnesium) also reduced HOMA-IR and also decreased fasting glucose concentrations.15 In other words, vitamin D supplementation yielded improvements in insulin sensitivity in women with PCOS.15
Biomarkers of oxidative stress and inflammation among women with PCOS have also been examined in RCTs with vitamin D intervention; overall, higher dose groups experienced improvements in oxidative stress and inflammation.16 For example, one 3-month study included in both meta-analyses15,16 investigated the impact of vitamin D supplementation with or without with metformin on metabolic profiles of insulin resistant, Iranian women with PCOS.17 This RCT randomized patients into three groups: “high dose” vitamin D (4,000 IU/d) + metformin, “low dose” vitamin D (1,000 IU/d) + metformin, or placebo + metformin. Following intervention, metabolic profiles were significantly improved in the high dose vitamin D group compared to the low dose and placebo groups.17
Specifically, the high dose vitamin D group experienced significantly lower total testosterone, lower prevalence of hirsutism, and lower high-sensitivity C-reactive protein (hs-CRP), a marker of inflammatory response.17 Additionally, significant elevations in total antioxidant capacity (showing improved free radical fighters) and sex hormone binding globulin (SHBG) were observed in the high dose vitamin D group, indicating improved body regulation of circulating hormones.17
Female-centric considerations for vitamin D status
There are many risk factors for vitamin D deficiency in women, which we have covered previously. One gender-based factor for some women, constructed by cultural and/or religious forces, may be partial or complete covering with clothing, and thus, limited exposure to sunlight and cutaneous synthesis of vitamin D.
Additionally, with the increased prevalence and public health awareness of skin cancer, more women are using sunscreen and limiting time in the sun. Because of less opportunity to receive vitamin D through the skin, clinicians should discuss the implications of low vitamin D status with their patients and promote practical ways to achieve and maintain healthy serum 25(OH)D levels– namely, vitamin D supplementation.
Genomic risk and PCOS
The actions of the active, hormone form of vitamin D [1,25(OH)2D] are mediated by the vitamin D receptor (VDR). And over 3% of the human genome is regulated by the VDR gene.18 That may not sound like a lot, but it translates into hundreds of protein-coding genes. With advances in genetic testing for various diseases, many patients may want to know if there is a genetic component to PCOS. One meta-analysis found that VDR Fokl and Taql polymorphisms were associated with an increased risk of PCOS in certain populations (e.g., Asians).18 Another meta-analysis found that VDR variants, Apal, Bsml, and Fokl, were associated with heightened risk of diseases related to insulin resistance, particularly in Caucasians with darker skin (i.e., from Saudi Arabia, India, Egypt, and Iran) and Asian populations.19
The good news is that even if the patient carries a VDR variant linked to PCOS, improving vitamin D status via lifestyle modifications (e.g., achieving healthy weight, incorporating sun exposure in moderation, and incorporating vitamin D sources in the diet) along with intervention via routine vitamin D supplementation has more impact on PCOS outcomes than genetic variations.
Dietary/nutrition considerations in PCOS
It is well recognized that lifestyle intervention is the cornerstone of treatment for patients with PCOS.20 First line PCOS treatment should include targeted lifestyle modifications that focus on weight management, including optimizing dietary approach and increasing physical activity. In fact, the good news is that a relatively low reduction in weight (~ 5 percent) can improve insulin resistance, hyperandrogenism, menstrual function, and fertility.20,21
Clinical consensus for dietary recommendations from the international consortium have focused on overall reduction in calorie intake and general healthy eating principles, with no one particular diet reported to have more favorable outcomes over another. Dietary guidelines and lifestyle recommendations are centered on achieving a healthy weight and managing metabolic and reproductive functions. The following recommendations have been shown via research to be successful nutritional management approaches for PCOS:21-24
More on the ketogenic diet for PCOS—initial data are promising, but not quite ready for prime time according to PCOS guidelines, though it is an active area of investigation. Other areas of active research include intermittent fasting and the fasting-mimicking diet.
Regardless of the dietary approach, “Weight loss should be targeted in all overweight women with PCOS through reducing caloric intake in the setting of adequate nutritional intake and healthy food choices irrespective of diet composition.”20
Improving vitamin D status in patients with PCOS
Individual nutrients of interest in PCOS research, such as vitamin D, were not specifically addressed in the 2018 international PCOS guidelines.6 However, because the growing body of research on vitamin D status and supplementation interventions in patients with PCOS is compelling, it is prudent for practitioners to partner with patients to assess their vitamin D status (via serum 25(OH)D concentration; sufficiency is defined as ≥ 30 ng/mL) and help them achieve and maintain vitamin D sufficiency through supplementation.10
Supplementation recommendations can be personalized based on periodic serum 25(OH)D measurements (e.g., it can take 3-4 months for 25(OH)D to reach a new steady state), and dosing depends on whether you are repleting a deficient state (6,000 IU/day or 50,000 IU/week for 8 weeks) or maintaining a 25(OH)D level in the normal range (at least 1,500-2,000 IU/day).10 However, it is important to remember that patients with overweight and obesity (common in PCOS) may need 2-3 times more vitamin D daily than their normal-weight counterparts.10
Optimal healthcare approach for patients with PCOS
A multidisciplinary, holistic, and personalized lifestyle medicine approach to care is the best practice for patients with PCOS. Collaboration and continuity of care with specialists across the PCOS spectrum has the greatest impact on outcomes and patient satisfaction.6,27
The evidence-based guidelines recommend lifestyle management as the first line therapy, with weight management being of utmost importance. Modest weight loss can net significant metabolic and hormonal improvements in patients with PCOS.20 Research indicates that weight management outcomes in women with PCOS are likely improved by the inclusion of the following factors: behavioral and psychological strategies, goal setting, self-monitoring, cognitive restructuring, problem solving, relapse prevention.28 Strategies that target improvements in motivation, social support, and psychological well-being are also key.28
Providing your patients with high-quality, multidisciplinary resources and referrals will improve their opportunity to receive support for the necessary lifestyle modifications.27 This may include consultations with fertility experts, endocrinologists, cardiologists, behavioral health specialists, registered dietitian nutritionists, or personal trainers, to name a few. Ask your patients what barriers to lifestyle management they may experience, and partner with them to champion key, gradual changes toward healing and wellness.
Although vitamin D supplementation recommendations are not yet included in the latest international PCOS guidelines, the evidence to date indicates that assessment and treatment of vitamin D deficiency and insufficiency among PCOS patients is likely a critical piece of the PCOS management puzzle. Vitamin D supplementation is the most pragmatic, beneficial, and clinically necessary approach when serum 25(OH)D levels are low, a scenario that applies the majority of patients with PCOS.
Sara Gottfried, MD is a board-certified gynecologist and physician scientist. She graduated from Harvard Medical School and the Massachusetts Institute of Technology and completed residency at the University of California at San Francisco. Over the past two decades, Dr. Gottfried has seen more than 25,000 patients and specializes in identifying the underlying cause of her patients’ conditions to achieve true and lasting health transformations, not just symptom management.
Dr. Gottfried is the President of Metagenics Institute, which is dedicated to transforming healthcare by educating, inspiring, and mobilizing practitioners and patients to learn about and adopt personalized lifestyle medicine. Dr. Gottfried is a global keynote speaker who practices evidence-based integrative, precision, and Functional Medicine. She recently published a new book, Brain Body Diet, and has also authored three New York Times bestselling books: The Hormone Cure, The Hormone Reset Diet, and Younger.
Kari Hamrick, PhD, RD is a registered dietitian with over 25 years of experience in nutrition and wellness and is the founder of Navigate Nutrition and Wellness, a private practice nutrition counseling center located in Gig Harbor, WA. Dr. Hamrick earned her PhD in nutritional sciences from Texas Woman’s University and received Adult Weight and Lifestyle Management certification from the Commission on Dietetic Registration. Kari has special training and experience in Mindfulness Based Eating Awareness Training (MB-EAT), women’s health issues, and the nutritional management of heart disease, eating disorders, and digestive health. Dr. Hamrick is currently completing a medical communication fellowship at Metagenics. Dr. Hamrick’s passion is helping individuals meet their nutrition and health goals with respect, open communication, and a sense of humor. She is also a yoga and dance instructor and enjoys learning and performing aerial acrobatic arts.
by Ashley Jordan Ferira, PhD, RDN
The importance of vitamin D in diverse organ systems and biochemical processes is ever-growing with novel research findings. From calcium absorption to extraskeletal health processes such as immune function- vitamin D is essential.
The role of vitamin D in pain management is a newer area of investigation that has not been fully established. It is estimated that 25.3 million American adults experience pain every day, with nearly 40 million experiencing some form of extreme pain.1 Annual costs associated with treating pain and pain-related symptoms are estimated to be higher than cancer and diabetes combined, reaching upwards of $600 billion per year.2 The striking number of Americans experiencing pain, combined with the associated financial burdens, underscores the need for clinically efficacious pain management methods.
Chronic non-specific widespread pain (CWP) including fibromyalgia (FMS) is associated with diffuse pain, reduced pain threshold, multiple points of tenderness, disability, and decreased quality of life. To better understand if vitamin D supplementation can significantly impact (CWP) including fibromyalgia (FMS), researchers, performed a systematic review and meta-analysis, the results of which were published in Clinical Rheumatology.3
Researchers comprehensively assessed databases for pertinent vitamin D trials. The authors focused on randomized controlled clinical trials evaluating the effects of vitamin D on CWP and FMS; 4 clinical trials met the inclusion criteria. After pooling the data from over 270 patients, regression, sensitivity and heterogeneity analyses were evaluated. Visual Analog Scale (VAS) of pain intensity was a major outcome measure.
Pooled results revealed a significantly lower VAS of pain intensity in CWP patients who received vitamin D treatment vs. those who received a placebo control. The analysis concluded that vitamin D supplementation decreased pain scores and improved pain symptoms.
Why is this Clinically Relevant?
Link to abstract
The female-centric 411 on this essential nutrient
by Ashley Jordan Ferira, PhD, RDN
Vitamin D research and daily news headlines are ubiquitous. PubMed’s search engine contains over 81,400 articles pertaining to vitamin D.1 Information abounds on vitamin D, but the vetting and translation of that information into pragmatic recommendations is harder to find. Evidence-based takeaways and female-centric recommendations are crucial for healthcare practitioners (HCPs), their female patients and consumers alike. Women are busy, multi-tasking pros, so practical, personalized takeaways are always appreciated. In other words, women need the “411” on vitamin D. Merriam-Webster defines “411” as “relevant information” or the “skinny”.2 So for all of you busy women, here’s the skinny on vitamin D. Let’s explore common questions about this popular micronutrient.
Q: Is vitamin D more important for younger or older women?
A: All of the above. Vitamin D plays a critical role in women’s health across all life stages, from fertility/conception, to in utero, childhood, adolescence, adulthood, older adulthood, and even in palliative care. Vitamin D is converted by the liver and kidneys into its active hormone form: 1,25-dihydroxyvitamin D. This dynamic hormone binds nuclear receptors in many different organs in order to modulate gene expression related to many crucial health areas across the lifecycle, including bone, muscle, immune, cardiometabolic, brain, and pregnancy to name a few.3
Q: I am a grandmother. Are my vitamin D needs different than my daughter and granddaughter?
A: Yes, age-specific vitamin D recommendations exist. As an essential fat-soluble vitamin, women need to achieve adequate levels of vitamin D daily. Age-specific Recommended Dietary Allowances (RDA) from The Institute of Medicine (IOM),4 as well as newer clinical guidelines from The Endocrine Society,5 provide helpful clinical direction for daily vitamin D intake and/or supplementation goals.
The IOM RDAs4 are considered by many vitamin D researchers to be a conservative, minimum daily vitamin D intake estimate to support the bone health of a healthy population (i.e. prevent the manifestation of frank vitamin D deficiency as bone softening: rickets and osteomalacia):
Infants (0-1 year): 400 IU/day
Children & Adolescents (1-18 years): 600 IU/day
Adults (19-70 years): 600 IU/day
Older Adults (>70 years): 800 IU/day
The Endocrine Society’s clinical practice guidelines5 recommend higher daily vitamin D levels than the IOM, with a different end-goal: raising the serum biomarker for vitamin D status [serum 25-hydroxvitamin D: 25(OH)D] into the sufficient range (≥ 30 ng/ml) in the individual patient:
Infants (0-1 year): At least 1,000 IU/day
Children & Adolescents (1-18 years): At least 1,000 IU/day
Adults (19+ years): At least 1,500 – 2,000 IU/day
Q: I am a health-conscious woman who eats a nutritious, well-rounded diet. I should not need a vitamin D supplement, right?
A: Not so fast. Daily micronutrient needs can be met via diet alone for many vitamins and minerals. Vitamin D is one of the exceptions, which is why an alarming number of Americans (93%) are failing to consume the recommended levels from their diet alone.6-7 Very few foods are endogenous sources of animal-derived vitamin D3 (cholecalciferol) or plant-derived vitamin D2 (ergocalciferol). Some natural vitamin D sources include certain fatty fish (e.g. salmon, mackerel, sardines, cod, halibut, and tuna), fish liver oils, eggs (yolk) and certain species of UV-irradiated mushrooms.8 In the early 20th century, the US began fortifying dairy and cereals with vitamin D to help combat rickets, which was widespread. For example, one cup (8 fluid ounces) of fortified milk will contain approximately 100 IU of vitamin D.
Even though some food sources do exist, the amounts of these foods or beverages that an adult would need to consume daily in order to achieve healthy 25(OH)D levels (> 30 ng/ml) is quite unrealistic and even comical to consider. For example, you would need to toss back 20 glasses of milk daily or 50 eggs/day to achieve 2,000 IU of vitamin D! In contrast, daily vitamin D supplementation provides an easy and economical solution to consistently achieve 2,000 IU and any other specifically targeted levels.
Q: I enjoy the outdoors and get out in the sun daily, so I should be getting all of the vitamin D that I need, correct?
A: Vitamin D is a highly unique micronutrient due to its ability to be synthesized by our skin following sufficient ultraviolet (UV) B irradiation from the sun. Many factors can result in variable UV radiation exposure, including season, latitude, time of day, length of day, cloud cover, smog, skin’s melanin content, and sunscreen use. Furthermore, medical consensus advises limiting sun exposure due to its established carcinogenic effects. Interestingly, even when dietary and sun exposure are both considered, conservative estimates approximate that 1/3 of the US population still remains vitamin D insufficient or deficient.9
Q: What factors can increase my risk for being vitamin D deficient? Are there female-specific risk factors?
A: Although the cutoff levels for vitamin D sufficiency vs. deficiency are still debated amongst vitamin D researchers and clinicians, insufficiency is considered a 25(OH)D of 21-29 ng/ml, while deficiency is < 20 ng/ml.5 Therefore, hypovitaminosis D (insufficiency and deficiency, collectively) occurs when a patient’s serum 25(OH)D falls below 30 ng/ml. The goal is 30 ng/ml or higher.
Ideally, vitamin D intake recommendations4-5 and therapy are personalized by the HCP based on patient-specific information, such as baseline vitamin D status, vitamin D receptor single nucleotide polymorphisms and other pertinent risk factors.
Common risk factors for vitamin D deficiency to look out for include:
-> Older age
-> Regular sunscreen use
-> Winter season
-> Frequent TV viewing
-> Dairy product exclusion
-> Darker skin (more melanin)
-> Not using vitamin D supplements
-> Malabsorption disorders (e.g. bariatric surgery, IBD, cystic fibrosis)
-> Liver disease
-> Renal insufficiency
-> Certain drug classes: weight loss, fat substitutes, bile sequestrants, anti-convulsants, anti-retrovirals, anti-tuberculosis, anti-fungals, glucocorticoids
-> Lastly, additional female-specific risk factors to look out for include exclusive breastfeeding while mother is vitamin D insufficient (can result in infant being vitamin D deficient) and certain cultural clothing that covers significant amounts of skin surface area (e.g. hijab, niqab).
Ashley Jordan Ferira, PhD, RDN is Manager of Medical Affairs and the Metagenics Institute, where she specializes in nutrition and medical communications and education. Dr. Ferira’s previous industry and consulting experiences span nutrition product development, education, communications, and corporate wellness. Ashley completed her bachelor’s degree at the University of Pennsylvania and PhD in Foods & Nutrition at The University of Georgia, where she researched the role of vitamin D in pediatric cardiometabolic disease risk. Dr. Ferira is a Registered Dietitian Nutritionist (RDN) and has served in leadership roles across local and statewide dietetics, academic, industry, and nonprofit sectors.
Food-Fortified Vitamin D3 More Effective than D2 at Raising Serum 25(OH)D Levels | Blog | Metagenics
by Ashley Jordan Ferira, PhD, RDN
A food fortification trial demonstrated that 600 IU of daily vitamin D3 had a significantly greater impact than 600 IU of daily vitamin D2 in elevating serum blood levels of 25-hydroxyvitamin D [25(OH)D].1-2
Vitamin D is essential for skeletal health and many emerging extraskeletal physiological processes, but remains one of the most common micronutrient dietary gaps, resulting in widespread hypovitaminosis D globally. Understanding how much vitamin D the body needs daily, in what form, and from what sources is still being discovered.
There are two forms of vitamin D: plant-based ergocalciferol (vitamin D2) and animal-based cholecalciferol (vitamin D3). D2 can be found in UV-irradiated mushrooms, certain fortified foods (breakfast cereals, margarine, and milk), dietary supplements, and vitamin D prescription medications. D3 is found in oily fish, egg yolks, fortified milk, and dietary supplements.4 Chemically, D2 and D3 are almost identical except for key side chain differences, with D2 having an additional double bond. D3 has been shown to have a higher affinity to the vitamin D binding protein, hepatic 25-hydroxylase (enzyme that converts vitamin D to the circulating 25(OH)D form) and vitamin D receptor. Whether these chemical and cellular differences translate into differential abilities in raising serum 25(OH)D, the clinical measure of vitamin D status, has been a hotly debated topic since the early 20th century.5
Research literature to date demonstrates a robust case gaining momentum for vitamin D3 and against vitamin D2 for supplementation.4-5 In particular, a 2012 systematic review and meta-analysis by of randomized controlled vitamin D supplementation trials in humans explored a head-to-head comparison of vitamin D2 vs. D3 in raising serum 25(OH)D; vitamin D3 was clearly shown to be more efficacious at raising and maintaining serum 25(OH)D levels than vitamin D2.4 Authors concluded that vitamin D3 may be considered the preferred choice for supplementation.4
Since natural sources of vitamin D (dietary input and UVB exposure from the sun) are limited, and a daily vitamin D supplementation regimen is a personal health decision, vitamin D fortification of the food supply is an important, strategic public health measure to help increase dietary vitamin D intake and improve status in the general population.6 Clarity is needed to elucidate whether D2 and D3 are equally effective sources for food fortification, since both forms are currently utilized in the food supply.6 A study by Tripkovic et al. helps to shed light on key differences.1
Results were published in The American Journal of Clinical Nutrition by Dr. Laura Tripkovic and colleagues from a randomized, double-blind, placebo-controlled food fortification trial that included 335 healthy South Asian and white European women aged 20–64 years.1 Participants were randomized to one of five groups:
1) Placebo: Placebo juice with placebo biscuit
2) D2J: Juice supplemented with 15 mcg vitamin D2 with placebo biscuit
3) D2B: Placebo juice with biscuit supplemented with 15 mcg vitamin D2
4) D3J: Juice supplemented with 15 mcg vitamin D3 with placebo biscuit
5) D3B: Placebo juice with biscuit supplemented with 15 mcg vitamin D3
Fifteen mcg of vitamin D is equivalent to 600 IU of vitamin D, which is the US Recommended Daily Allowance (RDA) for ages 1-70 years.7 The daily food-fortified intervention was 12 weeks long during the winter, and serum total 25(OH)D levels were collected at baseline, week 6 and week 12. Data analysis combined ethnic groups.
D3-fortified consumption was shown to be twice as effective as D2 in raising 25(OH)D serum levels in the body.1 While the placebo group experienced a 25% reduction in serum 25(OH)D levels over the course of the study, the D2J and D2B groups saw 25(OH)D increases of 33% and 34%, respectively. Most effective, however, were the D3 groups, with 25(OH)D increases in the D3J and D3B groups of 75% and 74%, respectively. The D3J group induced higher incremental increases in 25(OH)D levels: 16.9 nmol/L higher than the D2J group, 16.0 nmol/L higher than the D2B group, and 42.9 nmol/L higher than the placebo group.1 Both juice- and biscuit-supplemented vitamin D3 groups demonstrated similar results, with no statistical differences seen between D3J and D3B groups.1 Compared to white European women, the South Asian women demonstrated a greater increase in 25(OH)D levels in response to both D2 and D3, which was likely caused by their lower baseline vitamin D status.1
This study shows that modest supplementation levels (600 IU daily) of D3 in food and beverage sources twice as effective at raising serum levels of 25(OH)D than vitamin D2.1This study and previous supplementation studies may impact future policy and practice for vitamin D supplementation source. Additional research addressing dose response, bioactivity of D3 versus D2 and the impact of foods with high levels of vitamin D3 is needed.2
Why is this Clinically Relevant?