by Ashley Jordan Ferira, PhD, RDN
Vitamin D is essential- it helps absorb calcium, supports nervous and muscle tissue, and the immune system. Compared to normal-weight counterparts, vitamin D deficiency is more prevalent in those with obesity. In the US over one-third of adults meet obesity criteria.1
A study in The Journal of Clinical Endocrinology and Metabolism2 examined cellular mechanisms of vitamin D trafficking in metabolically dysfunctional adipose tissue as compared to normal adipocytes in conjunction with a vitamin D supplementation intervention in a randomized, controlled trial.
Ninety-seven male subjects completed the vitamin D intervention study. Fifty-four normal-weight and 67 obese males were initially randomized to receive either 50 mcg/week of 25-hydroxyvitamin-D3 [25(OH)D3] (2,000 IU/week equivalent) or 150 mcg/week of vitamin D3 (6,000 IU/week equivalent) for one year. Vitamin D sufficiency was defined as a 25(OH)D blood level > 20 ng/ml. This serum concentration is aligned with the National Academy of Medicine’s cutoff for vitamin D sufficiency.3
Vitamin D uptake, conversion and release were investigated in control (non-insulin-resistant) and insulin-resistant 3T3-L1 adipocytes, as well as in subcutaneous adipose tissue (SAT) samples from lean and obese participants. The release of vitamin D and its metabolites were induced with the addition of adrenaline. Expression of the vitamin D receptor and vitamin D conversion enzymes, 25-hyroxylase and 1α-hydroxylase, was also examined.
The research team elucidated key differences in cellular vitamin D trafficking effects and supplementation effects:
Why is this Clinically Relevant?
Link to Abstract
by Ashley Jordan Ferira, PhD, RDN
Autism spectrum disorder (ASD) is a complex neurodevelopmental syndrome with significant social, communication and behavioral deficits and challenges.1 No cure exists for ASD, although early interventions (birth to 3 years) can yield developmental improvements.1 ASD impacts approximately 1 in 68 children in the US and is 4.5 times more common in boys (1 in 42) than girls (1 in 189).2
Vitamin D’s extraskeletal roles are numerous, including its role as a neurosteroid, impacting both brain development and connectivity, and likely synaptic plasticity as well.3 Vitamin D is also one of the most common micronutrient deficiencies. Previous research has revealed associations between gestational and early childhood vitamin D insufficiency and ASD.4 This suggests that hypovitaminosis D represents a modifiable risk factor for ASD.4Furthermore, preliminary evidence demonstrates that gene variants related to vitamin D metabolism play a role in the pathophysiology of ASD.5 Robustly designed intervention trials have been scant.
The first double-blind randomized controlled trial (RCT) utilizing vitamin D3 supplementation in children with ASD was published in The Journal of Child Psychology and Psychiatry in 2018.6 The study included 109 Egyptian children (85 boys; 24 girls) 3-10 years of age with confirmed ASD diagnosis. The children were randomized to receive vitamin D3drops (300 IU D3/kg/day; not to exceed 5,000 IU/day) or matching placebo drops daily for 4 months.6 Serum 25-hydroxyvitamin D (25[OH]D) levels were measured at baseline and 4-months. For ethical reasons, children who were identified to have vitamin D deficiency (25[OH]D <20ng/mL) were excluded from the study and administered vitamin D supplementation by the study authors.6 Autism symptoms were assessed using validated measures completed by two different psychologists and a senior psychiatrist.6
Four months of daily vitamin D3 supplementation at 300 IU/kg/day:6
Following 4 months of vitamin D3 supplementation, improvements (all p <0.05, most p <0.01; as compared to placebo) were demonstrated in many core manifestations of ASD, including:6
This rigorously designed RCT is the first of its kind to demonstrate safety and efficacy of vitamin D3supplementation in children with ASD.6 Two previous open-label vitamin D3 supplementation studies also demonstrated improvements in ASD symptoms.7-8 Wide-scale studies are warranted to continue to critically ascertain the effects of vitamin D on ASD.
Why is this Clinically Relevant?
Link to Article
Food first, but fill the gap: The case for vitamin D supplementation
Ashley Jordan Ferira, PhD, RDN
If you can have a favorite nutrient, mine would be vitamin D.
Historically famous for its essential, classical role in calcium and phosphorus homeostasis and bone physiology (think rickets prevention), the past few decades of research have unveiled diverse, extraskeletal health roles for vitamin D, including but not limited to the immune system, cardiometabolic pathophysiology, cancer, pregnancy, etc.
Whether consuming vitamin D2 or D3 (FYI, the latter more potently impacts vitamin D status),1 vitamin D ultimately circulates in the 25-hydroxyvitamin D [25(OH)D] form (the clinical biomarker used to measure vitamin D status) and acts throughout the body as a pleiotropic hormone in its active form, 1,25-dihydroxyvitamin D [1,25(OH)2D].
Unlike other nutrients, this fat-soluble vitamin is obtainable via several unique routes: the skin with adequate UVB exposure, a handful of natural food sources, a few fortified foods, dietary supplements, and even prescription drugs.
The problem is that few foods naturally contain vitamin D (e.g., egg yolk, certain fatty fish, fish liver oil, and certain species of UV-irradiated mushrooms), and fortified foods offer relatively small amounts (e.g., 100 IU vitamin D per 8 oz cup of fortified milk or orange juice),2 so vitamin D supplementation becomes a strategic solution. In the eloquent words of pediatrician and vitamin D researcher, Carol Wagner, MD: “Something so simple- vitamin D supplementation- could improve the health status of millions and so becomes an elegant solution to many of our health problems today.”
If it’s possible to be defensive of a micronutrient, I am protective of vitamin D. Non-evidence-based rumors and negative media attention targeting vitamin D are common. Some of the misinformation is hype from anti-supplement camps who make broad, sweeping statements that lack scientific substantiation. But not all of the vitamin D myths originate from bias or lack of intellectual rigor. After all, who has time to keep up with the impressive, daily output of new vitamin D research? Clinicians certainly do not have the luxury of time, not in the current healthcare paradigm. Nevertheless, when inaccurate conclusions are propagated to patients about vitamin D and their health, that’s more harm than good. So, let me help out.
This blog series explores some of the most common vitamin D myths. Let’s tackle just 1 myth today:
Myth: I get enough vitamin D from food, so I don’t need a vitamin D supplement.
Can you meet your vitamin D needs from food alone? Well, that depends on how you define “needs.” Let’s talk about the 2 major (and quite different) sets of vitamin D recommendations.
First, the National Academy of Medicine (NAM), formerly known as the Institute of Medicine, provided vitamin D Recommended Dietary Allowances (RDAs) in 2010.3 Here’s how much vitamin D NAM says that we (Americans and Canadians) need based on bone health research (think rickets and osteomalacia prevention, calcium absorption, etc.):3
But I have a bone to pick (pun intended) with NAM’s vitamin D recommendations. I find them to be problematic, if not contradictory at times, for a few key reasons.
To start with, the RDA is by definition “the average daily level of intake sufficient to meet the nutrient requirements of nearly all (97-98%) healthy people.”4 Well, that misses the unhealthy people. Since 2/3rd of the country are overweight or obese5 and heart disease and cancer are the #1 and #2 causes of mortality in the US, respectively,6 one can extrapolate that the vitamin D RDAs do not apply to a decent chunk of the gen pop.
In fact, research indicates that overweight and obese individuals require more vitamin D than their lean counterparts,7 but the NAM recommendations fail to consider adiposity.
Second, lumping a toddler and 68-year-old grandmother in the same RDA category (i.e., ages 1-70 years) seems to lack nuance. Skeletal health is critical throughout life, but you cannot tell me that the vitamin D needs for the rapidly accruing skeleton in childhood and adolescence are no different than an adult or older adult’s skeletal needs.
Third, the RDAs for daily vitamin D intake are simply incongruent with the serum 25(OH)D cutoffs NAM also published in 2010. They provided the following 25(OH)D ranges:
The somewhat ironic problem is that the overly conservative vitamin D RDAs won’t get you into the 25(OH)D range that NAM defines for sufficiency. Regular UVB sun exposure (with adequate skin surface area, right latitude, right time of year, etc.) can raise serum D levels into sufficiency, except cutaneous vitamin D synthesis from sun is highly variable and limited for many. But 400-800 IU/day of vitamin D simply won’t do the trick. It’s like asking someone to fill up an 30-gallon fish tank and giving them a few cups of water to do the trick.
In the sage words of the late Bob Heaney, MD: “We’ve been able to show that the (vitamin D) RDA barely budges the blood 25-hydroxyvitamin D level.”8 Thanks to Dr. Heaney, who made invaluable research contributions to the field of vitamin D, we know that 100 IU/day of vitamin D increases serum 25(OH)D concentrations by approximately 1 ng/mL.9That means that 1,000 IU/day of vitamin D would raise 25(OH)D by about 10 ng/mL. Although weight status, age, and the patient’s baseline vitamin D status can variably impact the supplementation response, this “rule of thumb” can be used to roughly calculate vitamin D supplementation needs.
For example, let’s take a patient: me. I have limited UVB sun exposure and consume some foods that contain vitamin D (e.g., milk, eggs, salmon) but irregularly. My daily 5,000 IU vitamin D3 supplement has my serum 25(OH)D at 54 ng/mL. It stays between 50-60 ng/mL, which is in the sufficient range.
But I’m an anomaly. Nationally representative research backs up the fact that Americans are not getting adequate vitamin D from their diets.10-11 First, 93% of Americans 2 years and older are failing to consume at least 400 IU/day of vitamin D from diet alone, and this estimate includes fortified food sources.10 Even when diet plus sun exposure are both thrown into the mix, about 1/3rd of the US population has serum 25(OH)D levels associated with vitamin D insufficiency or deficiency.11 For more details on vitamin D deficiency and why it persists, check out this blog.
Dietitians (I am one) and other clinicians love to preach “food first.” That slogan is true but ignores research on key nutrient gaps. I prefer to say, “food first, then fill the gaps.” And in the case of vitamin D, the gap is practically guaranteed, except for the outlier patient who’s knocking back fish liver oils and irradiated mushrooms.
Lastly, a more current and scientifically and clinically nuanced set of guidelines exist. One year after the NAM recommendations were released, several of the world’s leading vitamin D researchers convened to review the evidence to date, resulting in the 2011 publication: Evaluation, Treatment, and Prevention of Vitamin D Deficiency: An Endocrine Society Clinical Practice Guideline.12
The US Endocrine Society’s conclusions are harmonious with the mindset of a clinician, who is tasked with addressing the vitamin D needs of unique patients. The guideline recommends higher daily vitamin D levels than NAM, with a different and logical purpose in mind: Raising serum 25(OH)D levels into the sufficient range (≥ 30 ng/ml):12
The guidelines even differentiate vitamin D needs based on adiposity: Children and adults who are obese may need 2-3 times more vitamin D daily than normal-weight individuals.12 Finally, the US Endocrine Society provides clear guidance for correcting vitamin D deficiency in all age groups, with repletion and maintenance dosing information, which is a topic that I will cover in a future blog.
Individual genetic differences for the vitamin D receptor (VDR) (i.e., gene polymorphisms like Cdx2, Apa1, Fok1, Taq1) are another important facet to weave into each patient’s unique vitamin D story, underscoring the prudence of a personalized lifestyle medicine approach to treat the individual.
No, you cannot satisfy your vitamin D needs from food alone. If you plan to raise and maintain your serum 25(OH)D level (the biomarker that indicates vitamin D status) in the sufficient range for skeletal and extraskeletal health, that will require daily vitamin D supplementation. Remember, 30 ng/mL is not the goal. It’s the cutoff for insufficiency.
Here’s a sneak peak at some of the additional vitamin D myths that will be covered in future blogs:
Do you have a question about the science and clinical application for vitamin D? Let me know by commenting below!
Ashley Jordan Ferira, PhD, RDN is Manager of Medical Affairs and 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.
Vitamin D deficiency and the need for practitioner intervention
by Sara Gottfried, MD and Lewis Chang, PhD
When I finished my medical training in 1998 at the University of California at San Francisco, I thought I knew everything about vitamin D, particularly vitamin D deficiency and insufficiency. I understood vitamin D was important for the efficient trafficking of calcium in the body, and that helps to keep bones strong, which was important for women’s health over the age of thirty when bone density begins to decline. What I learned in the subsequent twenty years is that vitamin D is both a hormone and a vitamin, and an essential nutrient for more than 400 biochemical jobs in the body. And I learned that what I knew in residency was the tip of the iceberg.
Further, I discovered that I inherited a gene for a faulty vitamin D receptor (VDR), which means my body doesn’t absorb and transport vitamin D well, so I tend to have low levels of vitamin D in my blood. This potentially puts me at greater risk for accelerated bone loss, osteopenia, osteoporosis, multiple sclerosis, and certain malignancies such as colorectal cancer. I’m not that unique in carrying the risky gene, but I’m getting ahead of myself. More later on the gene/environment interactions as they relate to vitamin D status, and whether you should be checking your patients for them. As I continue to identify my own knowledge gaps regarding vitamin D, I have become obsessed with teaching other practitioners and my patients about how persistent vitamin D deficiency and insufficiency continue to be despite the public initiatives to raise awareness. In this series on vitamin D, I want to share with you the importance of vitamin D to your health and that of your patients, starting first in this article with how vitamin D status is determined, how prevalent vitamin D insufficiency and deficiency have been in our population, what factors can affect circulating vitamin D levels, recommendations for your female patients since they are at greater risk of problems, and what proven actions to take to help improve your patients’ vitamin D status.
How is vitamin D deficiency defined?
Serum 25-hydroxyvitamin D [25(OH)D] level is widely used as a bio marker of a person’s vitamin D status, for it is the main circulating form of vitamin D and the best estimator of both endogenous vitamin D synthesis in the skin upon exposure to UV-B light and dietary intake of foods and supplements containing vitamin D.1 Therefore, the diagnosis of vitamin D deficiency is based on the measurement of circulating 25(OH)D levels.
However, there is no consensus among key opinion leaders for what is considered an appropriate cutoff for normal, desirable, and optimal serum 25(OH)D concentrations. As a result, different cut-off points have been used to define hypovitaminosis D (deficiency of vitamin D), ranging from 10 ng/mL (25 nmol/L) to 30 ng/mL (75 nmol/L).2-6
There is no consensus among professional societies, either. In 2010, Institute of Medicine (IOM)—renamed in 2016 as the National Academy of Medicine (NAM)—suggested that circulating 25(OH)D levels need to be at least 20 ng/mL (50 nmol/L) to prevent osteomalacia and maintain bone health in at least 97.5% of the population. Therefore, levels at or higher than 20 ng/mL (>50 nmol/L) are defined as vitamin D sufficient. Levels lower than 20 ng/mL (<50 nmol/L) but above 12 ng/mL (>30 nmol/L) are considered vitamin D insufficient and are inadequate for bone and overall health. Levels below 12 ng/mL (<30 nmol/L) are vitamin D deficient which can cause rickets in infants and children and osteomalacia in adults (Figure 1).7
Conversely, believing the IOM recommendations to be too conservative, the Endocrine Society released its clinical practice guidelines in 2011 in which vitamin D sufficiency, insufficiency and deficiency was defined as circulating 25(OH) levels above 30 ng/mL (>75 nmol/L), between 20-30 ng/mL (50-75 nmol/L), and below 20 ng/mL (<50 nmol/L), respectively (Figure 1).8 These recommended cut-off points are similar to the guidelines released by the Central European Scientific Committee on Vitamin D.9 The Endocrine Society also argued that, since any methodology for 25(OH)D measurement is subject to assay variability, targeting a higher 25(OH)D cut-off value may ensure that an individual meets the requirement for sufficient vitamin D levels with only minimal risk of vitamin D toxicity.8
These conflicting professional recommendations result in constant debate among researchers and confusion among clinicians about where the optimal 25(OH)D levels fall. Nevertheless, it is at least agreed upon that serum vitamin D levels less than 30 ng/mL are definitely insufficient and probably deficient for most people. I advise 50-75 ng/mL.
Figure 1. 25(OH)D recommendations by the Institute of Medicine (IOM) and the Endocrine Society.
How prevalent is vitamin D insufficiency and deficiency?
The prevalence varies depending on how vitamin D insufficiency and deficiency is defined. Another important factor that needs to be considered is how 25(OH)D is measured and how differences in the assay methodology (such as assay sensitivity and analytical variability) confound prevalence estimation.
Figure 2. Prevalence of vitamin D insufficiency and deficiency (%) from 1988 to 2010 in the U.S. using standardized serum concentrations of 25(OH)D.10Since 1988, the National Health and Nutrition Examination Surveys (NHANES) have periodically tracked nutrition status of adults and children in the U.S. via examining a nationally representative sample population. These estimates are highly valuable in assessing the trends of vitamin D status over time. However, different assays have been used to determine 25(OH)D levels between 1988 and 2010, from DiaSorin radioimmunoassay to reformulated radioimmunoassay to the more accurate chromatography-based assays. To minimize laboratory method bias and imprecision in these different assays, the Vitamin D Standardization Program—initiated by the US Office of Dietary Supplements in the National Institutes of Health in collaboration with the National Institute of Standards and Technology, Centers for Disease Control and Prevention, and Ghent University—was organized in 2010 to promote standardize 25(OH)D measurement using liquid chromatography-tandem mass spectrometry (LC-MS/MS).11 Also, equations were developed to help standardize data from older radioimmunoassays to LC-MS/MS-equivalent data.
The first paper that reported the temporal trends of vitamin D status in the U.S. using standardized 25(OH)D measurement was published in American Journal of Clinical Nutrition (AJCN) in 2016. They found that the prevalence of IOM-defined vitamin D insufficiency and deficiency (together as one category) was 30-32 percent from 1988 to 2006 and 26 percent from 2007 to 2010 (Figure 2; left). The prevalence was even higher when the Endocrine Society recommended cut-off point was used: 70-77 percent from 1988 to 2006, dropping slightly to 64-65 percent from 2007 to 2010 (Figure 2; right). Also, non-Hispanic blacks and Mexican Americans had much higher prevalence of vitamin D insufficiency and deficiency than non-Hispanic whites.10
Prior to the development of standardizing 25(OH) measurements, an earlier study also had tracked the prevalence trend in the same NHANES cohort and found an increase in vitamin D deficiency over time.1 Now, from the standardized data, we know the prevalence of vitamin D insufficiency and deficiency has been relatively stable. This discrepancy illustrates the importance of method standardization and having data expressed in LC-MS/MS equivalents for the most accurate interpretation of the prevalence trends.
This AJCN report also reported a small increase in vitamin D supplement use (≥ 600 IU/day) among women over time: 2.1% during 1998-1994, increasing to 19% during 2009-2010.
Vitamin D supplement users tend to be older (≥40 y/o) and non-Hispanic whites, Still, the majority remained to be non-users; at 70% during 1988-1994 and at 57% during 2009-2010.10
What are the recommended dietary intakes of vitamin D for women?
The recommended dietary intakes of vitamin D for women from the IOM and the Endocrine Society are compared in Table 1. IOM recommends 600 IU/day for those who are 9-70 y/o and 800 IU/day for those more than 70 y/o to maintain bone health in at least 97.5% of the population in those age groups. Pregnant and lactating women have the same requirement of 600 IU/day.
The intake levels recommended by the Endocrine Society are higher than IOM’s. For those who are 9-18 y/o, at least 600 IU/day is needed. However, in order to consistently achieve 25(OH)D of 30 ng/mL (75 nmol/L) preferred by the Endocrine Society, 1000 IU/day may be required. For those who are 19 y/o and older, including pregnant and lactating women, at least 1500-2000 IU/day may be required to maintain the blood levels of 25(OH)D to above 30 ng/mL (75 nmol/L).
Table 1. The recommended dietary intakes of vitamin D for women from IOM and the Endocrine Society.
*RDA (Recommended Dietary Allowance): the average daily dietary intake level that is sufficient to meet the nutrient requirement of 97.5% of healthy individuals in a group. **UL (Tolerable Upper Intake Level): the highest level of daily nutrient intake that is likely to pose no risk of adverse health effects to almost all individuals in the general population.
Are dietary intakes of vitamin D sufficient in women in the U.S.?
Overall no. Even among supplement users, the majority of women have insufficient intakes of vitamin D. Read more in this additional article debunking the myths of vitamin D.
The first study that presented national estimates of vitamin D intakes was conducted by the Office of Dietary Supplements and the National Institutes of Health based on NHANES 2005-2006 data.
The average vitamin D intake from diet alone was low in every age group (Table 2); the lowest being those 19-30 y/o (144 IU/day) and the highest 9-13 y/o (212 IU/day). When including vitamin D-containing supplement, vitamin D intakes somewhat increased, particularly among those 51 y/o and older (to approximately 400 IU/day).12 Even so, the intake still fell short of the RDA (600-800 IU/day) and way below the levels recommended by the Endocrine Society (1,500-2,000 IU/day).
Table 2. Mean vitamin D intake from the diet and from diet plus dietary supplements in women based on NHANES 2005-2006 data.12
*40 IU/day = 1 µg/day The low vitamin D intake seen during 2005-2006 was not a single event. A subsequent study that examined data from NHANES 2001-2002, 2003-2004, 2005-2006, and 2007-2008 confirmed the previous pattern: vitamin D intake from diet only remained extremely low across all populations and age groups, falling short of the RDA even when dietary supplement use was included.13
Further, this study identified certain sub populations that were at greater risks of insufficient vitamin D intakes. When comparing mean intakes by race, African Americans and Mexican Americans had even lower intakes than non-Hispanic whites. When stratifying by annual house income levels, low income was linked to lower vitamin D intakes. Further, those who were affected by obesity had the lowest intake levels compared with those who had normal body weight.13
What about dietary intakes of vitamin D in other countries?
Insufficient intakes of vitamin D is not just a phenomenon in the U.S. In fact, it is a global issue. For example, a study involving populations in representative Western countries (Germany, U.K., and the Netherlands) concluded that vitamin D intakes are below recommendations in a significant part of the population in these countries.14 A more recent overview of vitamin D status globally found that vitamin D deficiency occurred all over the world such as in the Middle East, China, Mongolia, and India.15
How much vitamin D intake is needed to improve vitamin D status in women?
The Women’s Health Initiative Observational Study (WHI-OS), one of the largest cohorts of postmenopausal women in the U.S., has detailed data on vitamin D intake and serum 25(OH)D level, which has allowed the investigators to address this question. Analysis of the data identified a more or less linear relationship between vitamin D intake and serum vitamin D status: every 100 IU increase in total vitamin D intake (diet and supplement combined) was associated with approximately 0.83 ng/mL (2.08 nmol/L) higher serum 25(OH)D levels. Also, total vitamin D intake was the main factor that determined vitamin D status.16
This dose-response observation is consistent with findings from VIDOS (Vitamin D Supplementation in Older Subjects) study, a 1-year randomized trial that investigated vitamin D intakes and serum 25(OH)D levels in healthy postmenopausal women.17 VIDOS study also found that vitamin D intake at 1,600 IU/day could achieve serum 25(OH)D of 30 ng/mL (75 nmol/L) in 97.5% of the participating women. This dosage level is in line with the recommendations from the Endocrine Society.
Is increasing sun exposure alone able to optimize vitamin D status?
Some insights can be gained from a study which investigated serum 25(OH)D levels in a group of healthy men who had just completed a summer season of extended outdoor activity such as landscaping, construction work, farming, or recreation. Compared with the general population, these were people who received some of the highest sun exposure—and with sufficient body surface area exposed and without sunscreen—during the season when UV-B radiation was the strongest. The study found that median serum 25(OH)D concentration in these subjects at late summer reached 48.8 ng/mL (122 nmol/L). However, even with ample summer sun exposure, the median serum 25(OH)D dropped to 29.6 ng/mL (74 nmol/L) by late winter, barely meeting vitamin D sufficiency (30 ng/mL) defined by the Endocrine Society.18
Latitude also determines whether one may obtain sufficient levels of vitamin D via sun exposure. One study compared sun exposure in two different cities, Miami (latitude 26 degrees N) and Boston (latitude 42 degrees N), and found that it’s possible to synthesize vitamin D via skin in all months in Miami but it’s very difficult to do so during winter in Boston.19
Therefore, for a very specific group of people such as landscapers, construction workers and farmers who don’t live in high latitude and don’t use sunscreen, their vitamin D level during summer would be sufficient even without dietary intakes of vitamin D. However, their healthy vitamin D status is not sustainable by end of winter if they don’t have additional sources of vitamin D. For the majority of the population—those who spend most of their daylight hours indoors (e.g., office workers), use sunscreen, have their body surface area covered up (e.g., hat, long-sleeve shirt and pants), or live a sedentary lifestyle, etc.—it is highly unlikely that sun exposure alone can increase serum 25(OH)D to sufficient levels even during summer, let alone the rest of the year.
What are other important factors affecting vitamin D status?
Key non-modifiable factors include age, sex, and race/ethnicity. Although the IOM, the Endocrine Society, and many other professional organizations around the world recommend intake levels based on age and sex, it does not mean that age and sex are the most impactful factors of vitamin D status. Race/ethnicity is another factor that one cannot change, either. However, many factors (besides vitamin D intake) that affect vitamin D status are behavior- and lifestyle-related and therefore modifiable.
A 2018 analysis based on NHANES 2001-2010 data has identified several factors and calculated adjusted prevalence ratios of vitamin D deficiency (<20 ng/mL or 50 nmol/L) and insufficiency (20-30 ng/mL or 50-75 nmol/L) in the general population:20
The link between heavier body weight and poorer vitamin D status is a more recent discovery but from the public health viewpoint its impact can be significant, especially when the obesity epidemic has shown no sign of slowing. Due to higher fat mass, a larger individual may simply need more ingestion or internal synthesis of vitamin D to reach the same concentration as a smaller individual.21 This hypothesis is strengthened by findings from a weight loss intervention trial involving postmenopausal women which demonstrated an increase in serum 25(OH)D levels after weight loss.22
The link between physical activity and vitamin D status may be related to other factors. Decreased physical activity level, especially outdoor types, is associated with reduced sunlight exposure which limits vitamin D synthesis from the skin.8Lower physical activity may also contribute to weight gain leading to lower serum 25(OH)D levels due to the effect of dilution. Therefore, increasing outdoor physical activity can improve vitamin D status via increased sunlight exposure and improved body weight.
Do genetic factors play an important role in determining vitamin D status?
Several genes encode proteins and enzymes that are involved in vitamin D metabolism. Understandably, genetic variations such as single nucleotide polymorphisms (SNPs) of these genes may influence vitamin D status.
The first genome-wide association study (GWAS) to identify common genetic variants that influence serum 25(OH)D levels was conducted in 2010 by the SUNLIGHT Consortium involving approximately 30,000 Caucasians from Europe, Canada and the U.S.23 This study identified four SNPs that were associated with lower 25(OH)D levels:
In 2018, the consortium was expanded to nearly 80,000 individuals (all Caucasians) from 31 epidemiological cohorts.28The study confirmed the previous four genetic loci and identified two novel loci for serum 25(OH)D levels:
However, this is an area of active research, and different genetic variations associated with vitamin D status are being discovered in other studies involving other study populations.32-36 Further, little is yet known on how genetic variants interact with other non-genetic factors. For example, one cohort study involving 1,200 postmenopausal women of European descent found that the association between 25(OH)D levels and certain SNPs in GC and CYP2R1 genes were stronger in summer months but not winter months, or in individuals with dietary intakes of vitamin D above 400 IU/day but not below.37 Also, a randomized controlled trial involving nearly 1,800 adults demonstrated that the increase in 25(OH)D after consumption of 1,000 IU/day vitamin D for 1 year was modified by certain SNPs in CYP2R1, CYP24A1, and VDRgene.38 These gene-environmental interactions and associations, once repeated in larger epidemiological studies and confirmed in large clinical trials, will have important public health implications. It will help determine whether individuals with certain genetic risk factors may indeed require higher amounts of vitamin D to achieve sufficient levels of 25(OH).
Institute of Medicine miscalculation leads to the wrong recommendation of 600 IU/day
As we wrap up, I would like to share with you an interesting article, published in 2014, which was titled “A Statistical Error in the Estimation of the Recommended Dietary Allowance for Vitamin D.” (I have included the hyperlink here in case you are interested in reading the whole open-access article.) In brief, researchers from School of Public Health, University of Alberta (Canada) described how IOM’s RDA for vitamin D was underestimated due to a calculation error. IOM estimated that 600 IU/day of vitamin D would achieve serum 25(OH)D above 20 ng/mL (50 nmol/L) for 97.5% of the population, but the authors re-examined the data and estimated that 600 IU/day of vitamin D would only achieve 10.7 ng/mL (26.8 nmol/L) in 97.5% of the population.39 This means that the dose needed to achieve 20 ng/mL (50 nmol/L) in the majority of the population would have been significantly much higher than 600 IU/day.
Following the publication, another group of researchers verified in another publication that IOM indeed had made a calculation error.40 Miscalculated RDA for vitamin D can have serious public health and clinical implications as the true vitamin D insufficiency and deficiency would have been severely underestimated based on the IOM definition. Many researchers are now calling for the IOM and public health authorities to redefine RDA for vitamin D (closer to what the Endocrine Society has proposed) to allow for appropriate public health and clinical decision-making. In the meantime, I recommend dosing vitamin D to achieve serum sufficiency by starting with the Endocrine Society guidelines, not IOM.
In the next series of articles, I will discuss how vitamin D status is related to women’s health, including current scientific data on the genetic influence of different disease outcomes, as well as common clinical issues we face as clinicians on the front lines.
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.
Lewis Chang, PhD is Scientific Editorial Manager of R&D at Metagenics. Dr. Chang received his PhD in Nutritional Sciences at University of Washington, along with his MS in Nutrition and Public Health from Teachers College, Columbia University and BS in Pharmacy from National Taiwan University. Prior to joining Metagenics, he conducted dissertation research and completed a research assistantship and postdoctoral fellowship at the Fred Hutchinson Cancer Research Center in Seattle, WA. Dr. Chang has authored or co-authored and managed the publication of over 30 peer-reviewed journal articles and numerous scientific abstracts and posters. He has quite a green thumb, enjoys opera, theater and jazz, and loves cooking, collecting art, and learning to play gypsy jazz guitar.
Racing Past Crohn’s: How Personalized Lifestyle Medicine Helped Lawson Aschenbach (Part 1) | Metagenics | Blog
Mental clarity, fitness, and good health are vital in racing, so a debilitating illness can threaten a professional race car driver’s career as well as his health. We sat down with seven-time professional sports car racing champion Lawson Aschenbach to learn how he used personalized lifestyle medicine to help manage his Crohn’s disease and return to the winner’s podium.
Let’s start with your professional background. How did you get into racing?I got into racing when I was 8 years old. My dad introduced my older brother and me to go-karting. It was a hobby at the time but quickly became my passion.
What is your schedule like? How much are you home? How often do you travel?I’m on the road between 150 and 200 days a year. That could be for race weekends, testing, or PR events. It’s difficult to stick to a schedule when you’re always traveling, so preparation has become an essential aspect of my life. I have containers for all the supplements I’m taking, and everything is premeasured before I leave for every trip.
When I’m racing, I’m either at the track or the hotel. I might be practicing, qualifying, or racing on those days, but I stick to a strict schedule. I go to bed at the same time every night; I wake up at the same time every morning. I make sure my health, focus levels, and body are in line to perform at a maximum level.
When I’m home, it’s a straightforward routine. I wake up, get breakfast, and go work out. There are a variety of exercises I use to keep myself in shape during and after the racing season. My afternoons involve office work and family. I try to spend as much time as I can with my wife and daughter. I’m enjoying fatherhood. It was an incredible experience bringing a baby into the world, and my daughter just turned 2 in December.
You were diagnosed with Crohn’s disease. How long were you having symptoms before you were diagnosed? How did your diagnosis come about?I initially started having digestive problems in middle school when I was 12 or 13 years old. After lunch, I would get embarrassing gas issues. It came out of nowhere and continued until I found the trigger, milk. Two cartons of milk were the daily lunch beverage at the time, and when I replaced it with something else, the issues stopped. It seemed strange to me that I could drink milk with no problems until that day.
Fast-forward to 2012 when I was experiencing continued gas, horrible bathroom experiences, dizziness, lethargy, a B12 deficiency, and insomnia. I wasn’t recovering from workouts either. It got to the point where this was starting to affect my career.
At one point I demanded a colonoscopy. I don’t know many people that would request one of those! But I had to get to the bottom of this, and sure enough, I immediately got a diagnosis of Crohn’s disease.
How old were you when you were finally diagnosed?Twenty-eight. My disease progressed quickly until the diagnosis. And to make matters worse, that was a rough time in my life because the racing world had taken a considerable hit during the economic crash. Stress became a part of my issues, and I believe it advanced all my symptoms at a much faster rate.
In some ways, I’m glad it happened because it forced me to figure out my health issues. Not only was it affecting my career, but also my life.
How did your illness affect your racing? How did it affect your life outside of racing?The most critical attribute in a driver is focus, and fitness is a big player in that ability. When you start getting tired, you start losing attention, and at 170 miles an hour, that can lead to disastrous results. Not to mention the fact that we’re in close quarters. We’re battling, trying to go for fast laps, and continuously searching for a split-second opportunity to pass someone.
When inflamed, I noticed my energy levels were declining. My workouts weren’t very promising, and the recovery times were slow. The combination of lack of sleep, lethargy, and consistent gastrointestinal issues created a lack of focus when I was in the car. When I was asked to do a two- or three-hour stint during an endurance race, I was having a hard time finishing it.
When things start happening, people take notice. It was a scary time. I knew I couldn’t continue this way for another season or else my career could end.
What was your experience with traditional medicine in treating Crohn’s disease?Immediately after my diagnosis in early 2012, I was prescribed an anti-inflammatory pharmaceutical drug. My doctor mentioned that we needed to get to the bottom of this, or I was on the path to resection surgery to remove part of my colon. Talk about scared straight!
He said I was going to take a pharmaceutical for the rest of my life while throwing out some stat that 90% of all Crohn’s patients never get to complete remission. It was a frustrating thought, but anyone that knows me understands that I never back down from a challenge!
How long was it before you were introduced to medical foods and personalized lifestyle medicine as a management option for Crohn’s?I did a significant amount of research after my diagnosis to try to figure out another way without taking pharmaceuticals. I was willing to do whatever it took. My symptoms were getting worse each day.
I reached out to a friend who learned of alternative methods to manage his battle with colitis. A nutritionist helped him manage his symptoms using diet and supplementation. He went from yearly hospital visits to living a more happy, healthy life.
I set up an appointment with the nutritionist, and that was my introduction to the world of lifestyle health plans and Functional Medicine. This was the turning point in my journey.
What was your experience with UltraInflamX Plus 360® Medical Food?Within 24 hours of using the product, it was life-changing. Almost all of my gastrointestinal issues subsided, and I immediately felt like a different person.
I had a new lease on life, and my mood changed accordingly. I felt that I could tackle any race in the world, and I had the health to back me up! I can say, without a doubt, that UltraInflamX Plus 360 changed my life!
How have your life and your racing changed since you switched to a personalized lifestyle medicine approach to managing Crohn’s?First and foremost, I have more energy. I’m recovering faster from workouts and races. I’m sleeping better, my focus level is at an all-time high, and, most importantly, my driving ability has been raised to a new level. Driving three-hour stints is no problem anymore, and I’ve been very fortunate to win four championships since being introduced to lifestyle medicine.
As a driver, we’re dealing with extreme temperatures-inside the car, it can be 130, 140 degrees. We don’t have a lot of driver comfort options, and our arms, legs, and head are constantly moving. It’s vital that you can zero in on what you’re doing, because you may only get one shot to pass someone during an entire race.
Nowadays, if there’s an opportunity, I’m going to take it. I’ve been fortunate to win a lot of races because of that desire and dedication. I feel I’m driving better than ever, and it’s showing in the results.
Lawson Aschenbach is a seven-time professional sports car racing champion. He started racing karts at the age of 8 and went on to win state, national, North American, and four Grand National Championships. In 2005, he finished on the podium in his first sports car race and then burst out onto the scene in 2006, winning the SPEED World Challenge GT Championship in his rookie year. Aschenbach has over 35 professional race wins and currently competes in the IMSA WeatherTech SportsCar Championship and Pirelli World Challenge Series.
“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” per se, 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 Sugars1. Beware of marketing geared toward dieters
2. Read ingredient labels, especially the first three ingredients
3. Beware of alternate forms and names for sugar
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.
We sat down with Joel Evans, MD to talk about Functional Medicine options for common women’s health issues. This is the first in a series.
Before we get started, can you tell me about your background? My background really is one of a conventionally trained OB-GYN. As I became interested in helping my patients in every way I could, it became clear to me that all I was trained in simply wasn’t enough.
The best example of this was a 26-year-old woman who I had the misfortune of diagnosing with breast cancer. She asked: Does it matter what I eat? The answer I gave was, “I don’t know; ask your oncologist.”
Her oncologist was very well known, trained at Harvard, and the answer came back: “It doesn’t matter what you eat.”
She asked me if I believed that, and I said, “Let’s find out for sure. Let’s have you meet with a nutritionist.”
She met with a nutritionist, who said you must avoid all sugar; sugar goes directly to cancer cells. I went to the medical library to do some research on sugar and cancer. I was shocked to discover that there were over 10,000 papers on cancer and sugar!
It was at that point that I realized that there’s more to taking care of people than is taught in medical school. That’s when I learned about Functional Medicine and met Jeff Bland and started speaking for Metagenics way, way back in 2002 or 2003.
What kinds of patients do you typically see? I see patients that I’ve seen forever as an OB-GYN who come to me for GYN care. Then I see patients that come to me because they want a Functional Medicine doctor. I also see the most complicated issues that are referred to me by my colleagues and healthcare practitioners that have been through IFM that know that I have a level of expertise that justifies the referral.
The patients you said you’ve seen forever, do you help guide them into the Functional Medicine realm? Or are they just there for their usual visits? I always try to guide them into the Functional Medicine realm. When I do their routine blood work, it is far more expansive than that ordered by a traditional doctor. I look for the subtleties in thyroid function. I look for subtleties in adrenal function. I ask probing questions like, How’s your mood? How’s your energy? How are you sleeping?
By asking those broader questions about issues that most OB-GYNs don’t inquire, I can then target the blood work to address them. When I go over the results, my patients are getting Functional Medicine care without knowing the term.
Are they open to that? Most are open to that. There are very few, maybe 2 or 3% that aren’t. The vast majority are, which is why they refer their friends and relatives to see me. I’m able to help them in all areas of their health.
How would treatment for fibroids and endometriosis differ from traditional medicine to lifestyle medicine? For example, what tests do you use, and can you manage these conditions with lifestyle adjustments?This is a big question to answer! The treatments in conventional medicine for fibroids and endometriosis are treatments that most patients don’t want. If fibroids are diagnosed during a routine exam, and there are no symptoms, the conventional treatment is to do nothing. Most patients aren’t happy with that. From a Functional Medicine perspective, there are a lot of things that we can do to prevent them from growing and becoming symptomatic.
Rarely do you find endometriosis without symptoms other than if you’re doing a pelvic exam and you feel a cyst, get an ultrasound on the cyst, and find out that it has qualities that are consistent with endometriosis. In that case, the only conventional interventions are birth control pills or surgery to get that cyst removed and see if there are other endometriosis lesions in the pelvis, where they can be destroyed with laser or electrocautery.
If patients have symptoms of fibroids, it can be a feeling of fullness, it can be abnormal bleeding, or it can be pelvic pain. There really are no long-lasting conventional treatments for fibroids other than some type of surgical procedure done by radiologists where they block the blood flow to the uterus or block the blood flow to the fibroids and the fibroids shrink.
What I do, the Functional Medicine approach, is totally different. I looked at the underlying driver of fibroid and endometriosis growth, and that has to do with estrogen. The Functional Medicine approach ensures there is not too much estrogen coming into, or being produced, by the body and that estrogen is being eliminated properly.
What are the sources of estrogen entering the body?It can be from foreign substances, so we can be taking chemicals in, compounds that become or behave like estrogen—those are called xeno-estrogens—that’s why eating organic is so important. We can also be drinking estrogen from our water. They have found estrogens from medications in the water.
The other way we can have too much estrogen is that we can be producing too much. For example, we can make too much estrogen through an ovarian cyst. Visceral adipose tissue produces estrogen. In addition, we know the enzyme that makes estrogen, aromatase, is actually inside of endometriosis tissue and inside uterine fibroids. Anything that stimulates aromatase will produce more estrogen. Two direct stimulators of aromatase are insulin and inflammatory prostaglandins. Therefore, the Functional Medicine approach includes normalizing insulin levels and reducing inflammation.
Another thing to do is look at how the gut functions. If there are unhealthy bacteria in the microbiome, they can produce an enzyme called beta-glucuronidase that leads to reabsorption of estrogen from the intestine. We have to make sure that we move our bowels regularly, because if there’s constipation, that leads to increased estrogen absorption.
We also have to make sure our liver is functioning well, that our cytochrome P450 detoxification enzymes are functioning well because estrogen is eliminated through those pathways.
You have a special interest in hereditary breast and ovarian cancer. What kind of risk assessment and prevention tools do you use with your patients?There are standard questions that are put out by National Cancer Institute and the National Institute of Health that we use to find out if patients are at increased risk for BRCA.
Then there are other questions that we ask. Dense breasts put a woman at increased risk for breast cancer. I also look at risk factors for other hereditary cancer syndromes, such as Lynch syndrome, where women are at increased risk of colon and gynecologic cancer. I also look for other, nongenetic reasons patients might be at increased risk for breast cancer, like being overweight, having increased adipose tissue, elevated insulin levels, or even being under stress.
I then also do a test called BREVAGen™, which can give patients a five-year risk analysis of breast cancer. That’s what’s called a genomewide association study. By looking at the gene frequency of approximately 77 genes, they can come up with a very accurate five-year risk of breast cancer. That means they are candidates for risk reduction medications in addition to a thorough Functional Medicine breast cancer risk reduction protocol.
Interested in learning how personalized lifestyle medicine can affect your life? Click here and select “Find a practitioner” to find a local personalized lifestyle medicine expert.
Your Brain on DHA
What is DHA?
Docosahexaenoic acid (DHA) is a long-chain omega-3 fatty acid—the most abundant of all the fatty acids most commonly found in the brain and eyes. But like many essential nutrients, DHA’s importance is often overlooked, and many Americans fall short of the recommended daily allowance (RDA) outlined by the US Department of Health.1,2 With all the cognitive, and other, benefits DHA has to offer, ensuring you get enough through your daily dietary intake is truly a no-brainer.
What are the benefits?
Not only does DHA account for over 50 percent of omega-3 fatty acids in the brain, it also turns on your brain’s growth hormone, known as the brain-derived neurotrophic factor (BDNF). This helps support the survival and function of existing neurons and also encourages new neurons and synapses to grow.3,4 Unfortunately, BDNF circulation slows down with age and can be stunted by stress and other lifestyle factors.5 That’s why upping your DHA is so important.
Although DHA is essential at every age, it’s especially crucial during three particular stages of life:
DHA can be helpful for baby’s development as well as mom’s recovery. A study showed that mothers who supplemented with omega-3s during pregnancy saw their children score higher on intelligence tests due to enhanced cognitive performance.6
For some mothers, pregnancy also takes a temporary toll on cognitive functioning and memory. Colloquially, it’s called “baby brain,” and it’s likely due to hormonal changes and the stressors placed on a woman’s body to meet the increased needs of her unborn baby. According to research, pregnancy can sometimes shrink brain tissue and cause long-term changes to brain structure.7,8 Recovery from pregnancy-induced brain changes can take years, but increased dietary intake of DHA has been studied to help support the regrowth of cells along the way, as well as promote healthy brain development in the baby.9
Babies and young children are growing every day, so it’s hard to understate the importance of DHA on brain development during this tender season of life.9 In fact, higher levels of DHA are associated with improved learning skills, while DHA deficiency in children has been linked to cognitive and learning disorders.10 That’s why making sure babies and toddlers get their fair share (500-700 mg daily)2 is a vital part of early brain development.
The benefits of DHA are enormously promising for older adults looking to keep their brains sharp and healthy. In a study of over 1,500 men and women over the age of 65, those with the lowest levels of DHA had significantly lower brain volumes than those with higher DHA levels and scored lower on tests measuring both memory and abstract thinking skills.11 On the flip side, studies show higher levels of DHA in the body (1,600 mg RDA for those age 51 and older)2 have also been associated with a decreased risk for brain-related chronic illness.11,12
DHA & gray matter
Our brains consist partly of something called “gray matter” (neural tissue that makes up a large amount of the central nervous system). Recent studies have supported a link between intelligence and the amount of gray matter in particular parts of the brain, which shrinks steadily in the years following adolescence. Though we naturally lose some brain volume over time, a higher intake of DHA is positively associated with gray matter volume and better cognitive function, even as we age.12
Where can I get it?
You can get some of your DHA in foods like fatty fish (salmon, mackerel, tuna, herring, and sardines) as well as flaxseed, chia seeds, and walnuts. But for vegans and vegetarians, as well as those with nut allergies, obtaining DHA through diet alone can be a challenge. It’s also important to be mindful of how often you eat certain kinds of fish due to high mercury content.
Supplementing with fish oils, a mainstay in many supplement regimens, can help fill in the gaps and give you the support you need for positive brain and cognitive development.1 There are many things to look out for when choosing a fish oil supplement, so keep these tips in mind while you shop.
This content is not intended as a substitute for professional medical advice, diagnosis, or treatment. Individuals should always consult with their healthcare professional for advice on medical issues.
Words can be used to allay or contribute to unwarranted fears. Often one hears phrases such as “whole-food” versus “synthetic” dietary supplements. What’s the difference? Let’s begin with basic terminology.
Vitamin CL-ascorbic acid is the naturally occurring form of vitamin C as found in many foods, including fruits such as oranges or cherries or plants such as rose hips. Each whole, unprocessed food that contains vitamin C also contains a unique blend of additional nutrients. No two foods will have vitamin C mixed with the exact same mixture of additional nutrients. There is no single “natural” vitamin C blend, and the additional nutrients do not change the biochemistry of the vitamin C itself.
While humans have lost the ability to endogenously synthesize vitamin C, certain mammals such as cows and sheep retain this ability. These animals produce vitamin C by a synthetic process--chemical synthesis from simple sugar. The vitamin C synthesized by these animals is not biochemically different than the vitamin C found in their food.
Vitamin C, as L-ascorbic acid, is natural vitamin C—regardless of endogenous chemical synthesis by an animal, chemically synthesized by the whole food, or synthesized for use in a dietary supplement.
Omega-3 fatty acidsOmega-3 oils as used in supplements are found in any number of forms (triglyceride, resterified triglyceride, phospholipid, emulsified, ethyl ester, free-fatty acid). While there may be minor bio availability differences among these forms, they are all forms of EPA/DHA synthesized from a natural source: no longer whole foods,being separated from the remainder of the nutrients found in fish (flesh, protein), but still starting from naturally occurring sources of EPA and DHA. Algal EPA and DHA are similar. While synthesized by certain microorganisms (certain Schizochytrium sp.) Algal EPA and DHA are created through synthesis of naturally occurring EPA and DHA by these microorganisms.
The human bodyThe human body is also a complex chemical factory, making or chemically synthesizing nutrients for use by the body. Proteins are prime examples. Humans do not absorb whole proteins from the diet; we digest them first (“degradation of a complex compound”), breaking proteins down to smaller peptides and free amino acids which then need to be synthesized (a “union of chemical elements”) into various other proteins, often structurally different from the food the individual amino acids came from. Further, the body chemically manufactures any number of nutrients from simpler compounds; glutamine and EPA/DHA are two examples of internal chemical synthesis.
Practically speaking, certain amino acids such as glutamine and certain fats (e.g.: EPA, DHA, GLA, arachidonic acid) would be considered synthetic, as they are “the union of chemical elements” converted by the body either into a more complex structure or degraded to a simpler one (fats are naturally elongated or shortened and hydrogenated or dehydrogenated).
What is the takeaway?
No one would consider nutrients chemically synthesized by the body as being synthetic or artificial. The discerning practitioner and discerning patient (consumer) need to look beyond words. Dig deeper to understand the concepts. If anyone says, “Hey, that’s synthetic,” or “We have whole-food nutrients,” that should raise a big caution.
This entry was posted in General Wellness and tagged Mark Kaye, Omega-3s, Vitamin C, Whole Foods on February 8, 2019 by Mark Kaye.
Methods to Help Manage Healthy Estrogen Balance
Hormonal balance is complicated. As women, we have a constant ebb and flow of hormones in our bodies that can greatly affect how we feel from day to day. Not only that, these hormones (estrogen, progesterone, and testosterone) work synergistically in the body to keep things running smoothly and hinge on a delicate balance that can easily be disrupted by lifestyle habits and environmental exposures. When that happens, we tend to feel, well, not quite right.
Estrogen dominance is the most common type of hormone imbalance—characterized by frequent headaches, mood swings and anxiety, bloating and weight gain, irregular periods, trouble sleeping, unexplained fatigue, worsened PMS symptoms, and more.1
Some of these symptoms may sound familiar to you. Maybe you’ve already been checked for estrogen dominance or hormonal imbalance. The good news is, there are a few things you can do to help manage estrogen dominance—starting today.
Living with estrogen dominance does not have to be a lifelong challenge. With these complementary methods, you can limit your exposure to xenoestrogens and help regulate your body’s natural hormonal balance.
If you have not had your hormone levels checked and show signs of estrogen dominance, please visit your healthcare practitioner.
*These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure, or prevent any disease.References: