Figure of mouse brain tissue from the substantia nigra; cells that are stained are dopamine producing.

Parkinson’s disease (PD) is a neurodegenerative disease, which means that the damage in the brain begins several decades before the symptoms appear. In PD, approximately 60% of a specific cell type in the brain dies before symptoms appear. The cells that die are dopamine-producing cells. Dopamine is a neurotransmitter, which is a chemical in the brain that help cells communicate with each other. Dopamine cells within the substantia nigra, an area of the brain, die in PD. In the figure above you can see dopamine-producing cells. PD was first described in 1817 by James Parkinson, and although the exact cause of PD still remains unknown, researchers and clinicians know that changes in our DNA play an important role. There is also an environmental component–for example, exposure to herbicides like paraquat induce PD in people. Another example of an environmental contributor is nutrition. 

Nutrition, specifically B-vitamins, have been implicated in the onset and progression of PD. Folic acid is an example of a B-vitamin, and it is well known for its role in preventing neural tube defects during early brain development. Additionally, folic acid also helps to lower levels of a chemical called homocysteine. High levels of homocysteine are present in PD patients who take levodopa (L-DOPA), a pharmaceutical drug that helps replenish dopamine in the brain. The breakdown of L-DOPA in the body requires methyl groups generated from folic acid, and this in turn increases levels of homocysteine.

Methylenetetrahydrofolate reductase (MTHFR) is a protein that breaks down folic acid to generate methyl groups, and people with reduced levels of this protein are reportedly more affected by PD. In a recent research study from our group we use a mouse model with reduced levels of MTHFR to study how the paraquat model of PD impacts onset and progression.

Our study found that reduced levels of MTHFR result in motor impairments in PD mice, and these impairments are characteristic of PD. Additionally, the PD mice were sick and had higher levels of inflammation in the substantia nigra. There were also high levels of oxidative stress, which is an imbalance of reactive oxygen and antioxidant production within a brain region closely connected to the substantia nigra. Higher levels of oxidative stress have been implicated in several neurodegenerative diseases. In terms of targeting oxidative stress through pharmaceuticals, there has not been much progress. Food stuffs such as red wine, green tea, and blueberries have been reported ro reduce levels of oxidative stress through their antioxidant properties, but more investigation is required.  

Nutrition is an important aspect of health. It is well documented that not all older adults absorb as many nutrients compared to their younger counterparts due to several factors, one being inflammation in the stomach. These recent research findings presented in this blog along with others suggest that adequate nutrition should be a component of health care for patients with PD.

A healthy, balanced diet is important for overall good health, but certain nutrients, such as protein, calcium, vitamin D, potassium, phosphorus, magnesium, and zinc, are particularly important for healthy bones.

Inadequate intakes of these nutrients increase the risk of bone loss and subsequent risk of osteoporosis, a condition characterized by low bone mineral density. Because dairy foods provide more of these bone-benefiting nutrients per calorie than any other food, consumption of dairy foods has been shown to be positively related to bone mineral density and reduced bone loss over time among a narrow sample of non-Hispanic whites. Although Puerto Rican adults (the second-highest represented subgroup of Hispanics in the United States) have a higher prevalence of osteoporosis and vitamin D deficiency than non-Hispanic whites, the impact of dietary choices on bone health in this population is poorly understood. Findings from a recent study conducted by Drs. Kelsey Mangano, Katherine Tucker, and Sabrina Noel (University of Massachusetts-Lowell) and published in the January 2019 issue of The Journal of Nutrition, reveal a unique dietary pattern that may detrimentally affect bone health.

To test their hypothesis, a total of 904 participants from the Boston Puerto Rican Osteoporosis Study provided diet information using a culturally tailored food-frequency questionnaire. For this study, dairy food groups included milk, yogurt, fluid dairy (milk + yogurt), cheese, cream and dessert dairy. Bone mineral density was measured using dual-energy X-ray absorptiometry, and vitamin D status was defined as sufficient or insufficient using a standard blood test.

The researchers found that higher intakes of modified dairy (milk + yogurt + cheese) and milk alone were significantly associated with higher bone mineral density. However, when compared by vitamin D status, total dairy, fluid dairy (milk + yogurt), and milk intake were significantly related to higher bone mineral density only among those with vitamin D sufficiency. Calcium and vitamin D intakes from all foods were lower than in the Dietary Guidelines, whereas protein intakes were higher compared with other adult populations. The scientists concluded that this unique dietary pattern may detrimentally affect bone health, because dietary protein intakes appear to be protective only under conditions of adequate calcium intake. Potential interventions to improve bone health should include dairy products in combination with public health messages to improve vitamin D sufficiency. Future studies should confirm these findings as well as assess culturally acceptable strategies to improve bone health among Hispanic adults.

Reference Mangano KM, Noel SE, Sahni S, Tucker KL. Higher Dairy Intakes Are Associated with Higher Bone Mineral Density among Adults with Sufficient Vitamin D Status: Results from the Boston Puerto Rican Osteoporosis Study. Journal of Nutrition. 2019; In Press.

https://doi.org/10.1093/jn/nxy234

A diet low in manganese may increase the risk for anovulation, or failure of the ovary to release an egg during a menstrual cycle. Approximately every 28 days, the female body prepares for pregnancy. About halfway through the cycle, the ovary will release an egg in response to hormonal changes. Disruptions in this process can result in infertility.

The BioCycle Study, completed at the University at Buffalo, was initiated to better understand the impact of diet and lifestyle on reproductive hormones and menstrual cycle abnormalities, including anovulation. The study assessed 259 healthy, regularly menstruating women over the course of two menstrual cycles. Data collected provide insight on health history and physical activity. Blood samples collected from participants at eight specific phases of the menstrual cycle are used to measure hormone levels and detect irregularities in ovulation. In addition, the collection of dietary data promotes evaluation of nutrient intake and reproductive health outcomes.

Researchers at the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) assessed the impact of dietary mineral intake on anovulation using data from the BioCycle Study. They found that a diet low in manganese, in reference to the recommended adequate intake (1.8mg/day for adult women), is associated with an increase in risk for anovulation.

How does this affect fertility?

Increasing intake of manganese is reasonable given that it is abundant in several readily available foods including teas, nuts, legumes, and whole grains But, before making dietary adjustments to improve fertility, the implications of these findings should be considered within the context of study design. In this case, anovulation was defined as sporadic, in that ovulation was only assessed over the course of two cycles and previous menstrual cycles occurred regularly. Consistent anovulation is a common cause of infertility, whereas intermittent anovulation is thought to have minimal impact on fertility, as menstrual cycles occurring before and after are believed to be healthy. However, a role for dietary manganese in fertility should not be ruled out as women with one sporadic anovulation have abnormal hormone profiles during preceding and future ovulatory cycles. This suggests ovarian dysfunction that may impact fertility.

Why does a diet low in manganese impair ovulation?

The exact function of manganese in human reproduction is not fully understood; however, studies rat studies indicate that the essential micronutrient may impact ovulation through its effects on the brain. Manganese accumulates in the hypothalamus, a region of the brain that regulates levels of reproductive hormones. Injection of manganese into the brain of prepubertal female rats increases levels of luteinizing hormone releasing hormone (LHRH), a reproductive hormone critical for ovulation.

Direct administration to the brain significantly differs from dietary intake of manganese; therefore further studies are required to determine the impact of manganese obtained from the diet. In addition, only a portion of manganese from the diet is absorbed, while the rest is excreted. Therefore, deficiency may be better reflected in manganese serum concentrations rather than dietary assessment. Furthermore, the body stores manganese in tissues including bone, liver, kidney, and pancreas. This suggests that a short-term dietary deficiency may not affect the overall balance of manganese in the body.

Nevertheless, observations on the association of dietary mineral intake and anovulation from the BioCycle Study are critical in stimulating further investigation into the impact of manganese on fertility.

According to the United Nations the aging population is growing and by 2050 the number of people aged 60 years old will reach 2 billion worldwide. With the aging population the prevalence of age-related disease is predicted to increase. An example of an age-related disease is neurodegeneration.  Dementia can be a result of several pathologies including increased levels of Lewy bodies (abnormal aggregates of protein in nerve cells), as seen in Parkinson’s disease.

Cerebrovascular disease is the second most common cause of dementia and is a result of  changes in blood flow to or within the brain. Blood flow in the brain can change because of hypertension, diabetes, smoking, and hypercholesterolemia. Patients with cerebrovascular disease experience cognitive impairment, specifically when trying to remember things or plan events/trips. It is important to note that symptoms can vary from patient to patient. A type of cerebrovascular disease is vascular cognitive impairment (VCI).

Nutrition is a modifiable risk factor for diseases of aging. As people age their ability to absorb nutrients from their diet decreases.  Several studies have reported that changes in B-vitamin absorption may play a role in the onset and progression of dementia. Additionally, a study by researchers in the United Kingdom shows that B-vitamin supplementation reduced brain volume loss in areas associated with cognitive decline. A recent international consensus statement from leaders in the field suggests that deficiencies in B-vitamin metabolism should be considered when screening dementia patients. My research using model organisms has tried to understand the disease processes associated with dementia.

Using a mouse model of VCI we have reported that deficiencies in folic acid, either dietary or genetic affect the onset and progression of VCI. Using the Morris water maze task we report that mice with VCI and folate deficiency performed significantly worse compared to controls. We assessed changes in the brain using MRI and interestingly found that folate deficiency changed the vasculature in the brains of mice with VCI. Because of either a genetic or dietary folate deficiency all the mice had increased levels of homocysteine.

Our results suggest that it is not elevated levels of homocysteine making the brain more vulnerable to damage, but the deficiency in folic acid, either dietary or genetic, that changes the brain. In the cell folic acid is involved in DNA synthesis and repair as well as methylation. These are vital functions for normal cell function. Therefore, reduced levels of folate may be changing the cells in the brain and making them more vulnerable to certain types of damage. We think that high levels of homocysteine may just be an indication of some deficiency (e.g. reduced dietary intake of folic acid). Maintaining normal levels of homocysteine are needed, since studies in humans have shown that elevated levels of homocysteine are a risk factor for neurodegenerative diseases and that reducing them is beneficial.

 

 

Folic acid is a B-vitamin and is well known for its role during early neurodevelopment. It promotes the closure of the neural tube in utero. The neural tube in the developing embryo is the first step to forming the brain and spinal cord. If the neural tube does not close, it can lead to neural tube defects (NTDs), such as spina bifida. Women of child bearing age are recommended to supplement their diet with 0.4 -1 mg of folic acid daily. Additionally, to reduce the number of NTDs mandatory folic acid fortification laws were put into place in 1998 in the US and Canada, as well as other countries around the world. In response to mandatory fortification, there has been a reduction in the number of NTDs in both Canada and the US.

Recently, maternal over supplementation of folic acid has raised some concerns.  Over supplementation is defined as ingesting over 1 mg of folic acid daily. There has been an increase in over supplementation of folic acid in the US and Canada where mandatory folic acid fortification laws are in place and supplement use is high. Epidemiological studies have reported that too much folic acid has been associated with increased risk of cancer. Interestingly, too much maternal folic acid intake has been associated with autism spectrum disorder, but the data is not clear as other studies have reported protective effects. Furthermore, too much maternal folic acid has been reported to change neurodevelopment in animals.

A recent published study investigated whether too much maternal folic acid is associated with changes in the neurodevelopment of offspring. Using a mouse model of maternal over supplementation of folic acid the authors report that male offspring from mothers that were fed high levels of folic acid had impaired memory and brain development.  The amount of folic acid in the diet of mothers was 20mg/kg to model over supplementation in humans. Animals from mothers with over supplementation of folic acid did not remember seeing a familiar object as well as control animals did. Furthermore, they had reduced levels of a neurotransmitter that is important in learning and memory called acetylcholine.

These are some of the first results showing how maternal over supplementation with folic acid may affect early neurodevelopment. We recently published an up-to-date review of how maternal over supplementation of folic acid impacts offspring neurodevelopment.  Our comprehensive analysis includes studies from human populations as well as basic science studies to understand how things in the brain as well as behaviors are changing when mothers are supplementing with too much folic acid.  More studies are required to understand the full impact of how maternal over supplementation affects offspring neurological development. As someone wise once said, everything in moderation.

 

Calcium is traditionally considered the bone-health nutrient. This is because 99% of calcium is contained within the bone, in which calcium creates a mineral complex with phosphate (hydroxyapatite), giving bone its characteristic strength and function. However, besides forming part of bone, calcium is also involved in other functions, such as muscle function, nerve transmission, intracellular signaling, and others.

Bone is a very dynamic organ in which the rate of formation and resorption (or destruction) is different throughout the lifespan. During childhood and adolescence, the rate of formation is higher than the rate of resorption, leading to maximum bone gain. In older adults these rates are switched, causing loss of bone. This bone loss may lead to osteopenia, osteoporosis, and an increased risk of bone fractures.

Is an increased intake of calcium associated with reduced risk of fractures?

As a way to prevent bone loss and fractures in middle-aged and older adults, there is usually a push from public health initiatives and healthcare professionals to increase the intake of calcium. However, an increased intake of calcium (dietary + supplements) may not necessarily lead to fewer fractures. Two of the most recent systematic reviews and meta-analyses showed that increasing dietary calcium and the supplementation of calcium (and vitamin D) did not reduce the risk of fractures. However, this remains controversial as a previous meta-analysis showed that the supplementation of calcium and vitamin D was associated with a 15% risk reduction in middle-aged and older adults (community-dwelling and institutionalized).

 The use of calcium supplements may lead to a higher risk of cardiovascular disease

The hypothesis is that an increased intake of calcium may lead to a positive calcium balance (intake lower than output in urine + feces), in the absence of increased bone formation. This positive calcium balance may lead to the calcification of tissues other than the bone, such as the vasculature, increasing the risk of cardiovascular disease. However, this association remains controversial. A sub-analysis of the Multi‐Ethnic Study of Atherosclerosis (MESA), showed that those that had higher dietary calcium intake (without supplements) had a lower risk of coronary artery calcification, while those that were taking supplements had a higher risk. However, the National Osteoporosis Foundation and the American Society for Preventive Cardiology suggested that calcium intake (diet + supplements) that does not exceed the tolerable upper level of intake of 2000 to 2500mg/d is not associated with cardiovascular outcomes, and should be considered safe.

Special caution of high intake of calcium in subjects with reduced kidney function

A high intake of calcium, particularly those that use calcium supplements, may represent a problem for those with reduced kidney function, as they may not be able to excrete the extra calcium. In a study by Hill and collaborators, a calcium intake of 2500mg (1000 mg through diet + 1500mg from calcium carbonate), compared with a dietary calcium intake of 1000mg, led to 500mg of calcium retention in patients with reduced kidney function. Similarly, Spiegel and collaborators compared a diet with 800mg vs. 2000mg of calcium in subjects with normal and reduced kidney function. In those on the 2000mg calcium diet, there was a positive calcium balance, which was more marked in those with reduced kidney function. With these results, a calcium intake higher than 800-1000mg (diet + supplements) should be avoided in those patients with a reduced kidney function to prevent calcifications of tissues other than the bone.

Should health care professionals recommend a high intake of calcium?

The current evidence, in middle-aged and older adults, does not seem to support high calcium intakes (above the tolerable upper level) for the prevention of fractures. Additionally, high calcium intakes achieved with the use of supplements may be associated with increased risk of cardiovascular disease. However, the use of supplements may be useful for patients that have low calcium intake. Finally, special attention should be taken in patients with reduced kidney function, as a high intake (diet + supplements) may lead to an increased risk of cardiovascular disease.

 

The popularity of the essential polyunsaturated omega-3 fatty acids (O3FA) is on the rise. In 2017, O3FA achieved a spot on the top 20 foods and ingredients list that Americans are adding to their diets (The Hartman Group). In addition, the global fish oil market is expected to reach a whopping 4.08 billion dollars in the next four years!  The proposed health benefits are likely the driving force behind the increasing demand.

Despite their booming popularity, a large percentage of adults are not meeting the O3FA recommended intake. There are three primary O3FAs with distinct characteristics: alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Although commonly grouped under the umbrella term O3FAs, are all O3FAs created equal?

Unique Characteristics of O3FAs

Omega-3 fatty acids cannot be sufficiently produced in the body earning them the title of “essential fatty acids.” The plant-derived omega-3, ALA, is the parent precursor to EPA and DHA. Unfortunately, the conversion rate in our bodies is very low.  It is important to realize that in the process of metabolizing ALA to EPA and DHA, a series of anti-inflammatory markers are produced (leukotrienes, prostaglandins and thromboxane). As these anti-inflammatory metabolites are beneficial, direct EPA and DHA consumption is needed to meet bodily requirements.

Independent and Complementary Health Benefits

The majority of current research focuses on the health benefits of marine fatty acids.  DHA and EPA consumption portray an array of shared and complementary benefits related to the treatment of cardiovascular disease, depression diabetes, sleep disorders and more. DHA is more significantly associated with decreases in resting heart rate, blood pressure and with improvements in cellular membrane health due to its additional double bond and longer carbon chain. Increased cellular levels of EPA have been shown to benefit coronary heart disease, hypertension and to decrease inflammation. EPA and DHA are both associated with reduced gene expression related to fatty acid metabolism, reduced inflammation and oxidative stress.

Specific supplementation of ALA is not consistently associated with cardiovascular health. Although plant-derived ALA can be easily substituted in for excess omega-6 fatty acids (O6FAs). Research has shown that by reducing the O3FA:O6FA ratio, you can decrease bodily inflammation, increase anti-inflammatory markers and more efficiently utilize EPA and DHA.

An ALA, EPA and DHA-Rich Diet

The 2015-2020 Dietary Guidelines for Americans recommends that healthy adults consume at least 8 ounces of a variety of non-fried fatty seafood per week. For EPA and DHA requirements, the American Heart Association recommends fatty marine sources containing 500 mg or more of EPA and DHA per 3oz cooked serving (e.g., salmon and tuna).   ALA is the most commonly consumed O3FA in the Western diet as it is found in plant-based foods (e.g., dark green leafy vegetables, walnuts, canola oil, flax seed). Unlike EPA and DHA, an Adequate Intake (AI) level is established at 1.6 g/day and 1.1 g/day for men and women respectively.

The Final Verdict 

The wide range of benefits stemming from marine O3FAs indicates the importance of regular consumption of fatty seafood and EPA and DHA-containing products.  The incorporation of plant-derived ALA may serve more importantly as a substitute for omega-6 fatty acids to reduce bodily inflammation, decrease the high O3FA:O6FA ratio typically observed in the Western diet, and to help elevate EPA and DHA levels in the body. EPA and DHA may be featured as the health promoting “dynamic duo,” but ALA is still invited to the party!

 

References

1.         Yanni Papanikolaou JB, Carroll Reider and Victor L Fulgoni. U.S. adults are not meeting recommended levels for fish and omega-3 fatty acid intake: results of an analysis using observational data from NHANES 2003–2008. Nutrition Journal 2014.

2.         Harris WS, Mozaffarian D, Lefevre M, Toner CD, Colombo J, Cunnane SC, Holden JM, Klurfeld DM, Morris MC, Whelan J. Towards establishing dietary reference intakes for eicosapentaenoic and docosahexaenoic acids. J Nutr 2009;139(4):804S-19S. doi: 10.3945/jn.108.101329.

3.         Frits A. J. Muskiet MRF, Anne Schaafsma, E. Rudy Boersma and Michael A. Crawford. Is Docosahexaenoic Acid (DHA) Essential? Lessons from DHA Status Regulation, Our Ancient Diet, Epidemiology and Randomized Controlled Trials. Journal of nutrition 2004;134.

4.         Mozaffarian D, Wu JH. (n-3) fatty acids and cardiovascular health: are effects of EPA and DHA shared or complementary? J Nutr 2012;142(3):614S-25S. doi: 10.3945/jn.111.149633.

5.         Bork CS, Veno SK, Lundbye-Christensen S, Jakobsen MU, Tjonneland A, Schmidt EB, Overvad K. Dietary Intake of Alpha-Linolenic Acid Is Not Appreciably Associated with the Risk of Ischemic Stroke among Middle-Aged Danish Men and Women. J Nutr 2018. doi: 10.1093/jn/nxy056.

6.         Evangeline Mantzioris MJJ, Robert A Gibson and Leslie G Cleland Differences exist in the relationships between dietary linoleic and alpha-linolenic acids and their respective long-chain metabolites. Am J Clin Nutr 1995;61:320-4.

7.         Agriculture. USDoHaHSaUSDo. 2015 – 2020 Dietary Guidelines for Americans. 8th Edition. December 2015.

Vitamin D, also known as cholecalciferol, plays an important role in bone health and muscle strength and is essential for the prevention of rickets (1). Cholesterol is a precursor of Vitamin D, which is endogenously produced in the body when ergosterol is exposed to UVB sunlight through the skin. It is also found in eggs, fatty fish and supplements (1).

A recent study by researchers in Japan found that higher levels of vitamin D may lower the risk of liver cancer. The study conducted by researchers at the Center for Public Health Sciences at the National Cancer Center in Tokyo suggests that people who suffer from low levels of Vitamin D may be at an increased risk for many different types of cancers; however the overall body of evidence is mixed (2,3).

This latest study was published in BMJ and explored biologically active forms of vitamin D in blood samples of over 30,000 middle-aged adults across Japan in the early 1990s. The follow-up for individuals was over a 16-year period. This analysis was based off a sample of 3301 participants who developed cancer during the study and 4044 randomly selected participants, of whom 450 developed cancer. The research team found higher levels of circulating vitamin D led to lower risk for cancers, overall, after controlling for age, sex, smoking status and family history of cancer. They also controlled for seasonal differences in circulating vitamin D. They did not find differences in the effect of vitamin D by sex; however, authors noted that participants in the lowest quartiles of vitamin D status had a 22% higher risk of cancer when compared to those in the highest quartiles. Additionally, they noted a 50% lower risk of liver cancers for those in the highest vitamin D group compared to the lowest, after adjusting for diet.

Vitamin D status was only measured at one point during follow-up, which serves as an important limitation. Additionally, inherent selection bias means that participants in the study may have been more health-conscious than the public at large. The number of rare cancer cases in the cohort was also small.

It is important to note that these latest findings apply primarily to Asian populations and higher levels of Vitamin D in these communities may lower risk for cancer; however, these findings cannot be translated across the board. It is important for those at risk of sun burns to avoid direct unprotected contact with the sun, which is a known risk factor for skin cancers. Additionally, lower levels of vitamin D may be an indication of poor health, overall (2,3).

Other health benefits of vitamin D have been seen in meta-analyses that have found a 31% reduction in falls among those supplemented with vitamin D. It also plays a role in improving the body’s response to infection among patients with cystic fibrosis (4). For populations in the US, vitamin D deficiency remains a problem in populations including African American communities, where according to the National Health and Nutrition Examination Survey (NHANES), 60% of people suffer from low levels (5,6). Through fortification of dairy products and supplementation, these numbers have reduced; however, greater attention including additional research is needed to reduce risk of deficiency, with added benefits to risk reduction for other health conditions, including cancers.

References:

  • Khazai, N., Judd, S.E. & Tangpricha, V. (2008). Calcium and vitamin D: skeletal and extraskeletal health. Current Rheumatology Reports, 10(2), 110-117.
  • Budhathoki, S., Hidaka, A., Yamaji, T., Swada, N., Tanaka-Mizuno, S., Kuchiba, A., Charvat, H., Goto, A., Kojima, S., Sudo, N., Shimazu, T., Sasazuki, S., Inoue, M., Tsugane, S., Inoue, M., Tsugane, S., & Iwasaki, M. (2018). Plasma 25-hydroxyvitamin D concentration and subsequent risk of total and site specific cancers in Japanese population: large case-cohort study within Japan Public Health Center-based Prospective Study cohort. The British Medical Journal, 2018, 360. https://www.bmj.com/content/360/bmj.k671
  • Davis, N. The Guardian, Nutrition. (2018) Retrieved from: https://www.theguardian.com/science/2018/mar/07/vitamin-d-may-offer-protection-against-cancers-study-says
  • Pincikova, T., Paquin-Proulx, D., Sandberg, J.K., Flodstrom-Tullberg, & M., Hjelte, L. (2017). Clinical impact of vitamin D treatment in cystic fibrosis: a pilot randomized controlled trial. European Journal of Clinical Nutrition, 71, 203-205.
  • Jain, R.B. (2016). Recent Vitamin D data from NHANES: Variability, trends, deficiency and sufficiency rates and assay compatibility issues. Journal of Advanced Nutrition and Human Metabolism, 2. https://www.smartscitech.com/index.php/JANHM/article/view/1208
  • Avenell, A., Mak, J.C., & O’Connell, D. (2014). Vitamin D and vitamin D analogues for preventing fractures in post-menopausal women and older men. Cochrane Database of Systematic Reviews, 14(4).

By: Sheela Sinharoy, MPH

Sunday began with a symposium titled, Delivering Nutrition Interventions to Women during Pregnancy: Beyond Individual Interventions to Comprehensive Antenatal Guidelines and Care. A series of speakers made clear that as antenatal care (ANC) models continue to evolve, there is plenty of room for improvement to provide a positive pregnancy experience for women and their families.

ANC is not meeting its potential. This was the conclusion of the first speaker, Erica Phillips. She discussed the model of focused ANC (FANC) recommended by the World Health Organization (WHO), which involves 75-80 tasks for an intake visit and 60-65 tasks for each follow-up. She explained that following these recommendations would require an estimated 30-40 minutes for a first visit and 20 minutes for a follow-up. Even when recommended tasks are completed, quality of care may still be low. Ms. Phillips stated that “where FANC has been adopted, success has been limited.”

Still, ANC can be an effective platform for breastfeeding promotion, according to the next speaker, Mduduzi Mbuya. He presented a case study from the Sanitation, Hygiene, Infant Nutrition Efficacy (SHINE) trial in Zimbabwe. The country faces a critical shortage of health workers, with only 9.8 skilled health workers per 10,000 people (as compared to a ratio of 117:10,000 in the USA). SHINE therefore engaged community-based village health workers and found that the prevalence of exclusive breastfeeding at six months of age increased from 23% to 68%. Dr. Mbuya attributed this result primarily to strong fidelity of implementation by village health workers.

Micronutrient supplementation is another important component of ANC, and Kate Dickin spoke about a trial of calcium supplementation in Kenya and Ethiopia. There, researchers found that women were motivated and willing to take calcium supplements as recommended and that most women sustained their adherence to the supplements through the six-week study period and said they would continue through the end of their pregnancies. Dr. Dickin attributed this largely to the intervention’s behavior change communication strategy, which was based on extensive formative research and addressed context-specific motivators and barriers.

Next, Catharine Taylor spoke about the way forward and the need for integrated, women-centered models of care. She said that ANC models should take the local context into account; have all goods and personnel in same physical space; provide clear and consistent guidelines, training and supervision to health workers; provide demonstrations and encourage active engagement and discussion; provide incentives and support; and implement women-held records and integrated health registers. As examples, she described the Centering Pregnancy model and women’s support groups, which have shown promise in a number of developing country settings.

Finally, Rebecca Stoltzfus closed the session, emphasizing the need for more community-based evidence, especially looking at “packages of ANC that are contextually adapted to be delivered in the most effective ways.” Thus, symposium attendees walked away with a substantial research agenda for the strengthening of antenatal guidelines and care.

 

By: Mary Scourboutakos

Neural tube defects are a type of birth defect—affecting the brain, spine or spinal cord—that result from suboptimal folate status.
Folate is a B vitamin that’s naturally found in legumes (like chickpeas, lentils, pinto and kidney beans), seeds, leafy greens (like spinach, collard greens and romaine lettuce) and other vegetables such as asparagus, brussels sprouts and broccoli.

The problem is, people don’t eat enough of these foods. As a result, for many years, pregnant women were at risk for folate deficiency and hence, neural tube defects.

Prenatal supplements were the original solution to this problem as one of their prime ingredients is folic acid, the synthetic form of folate. However, they’re not a fool proof solution because neural tube defects form within four weeks of conception, often before women know they’re pregnant, and thus, before they start taking their supplements.

As a result, in the late 1990s folic acid was mandatorily added to white flour and enriched grain products to ensure that pregnant women would get enough folate, irrespective of whether they take a supplement.

Problem solved? Sort of…

Back in the early 1990s when discussions regarding the addition of folic acid to the food supply were taking place, it was suggested that after fortification was implemented, the dose of folic acid in prenatal supplements should be revised to prevent excessive intakes. The new problem is…the doses were never revised.

Currently, marketed prenatal supplements usually contain 1000 micrograms of folic acid, which is the daily upper limit for folic acid. Meanwhile, it’s recommended that pregnant women should consume about 400 micrograms of folic acid per day for neural tube defect prevention.

With mandatory fortification, three-quarters of a cup of cereal can provide greater than 400 micrograms of folic acid. So if you add a prenatal supplement to a bowl of cereal at breakfast, some bread at lunch, and pasta for dinner, you’re consuming a lot of folic acid!

According to Dr. Deborah O’Connor, a Professor from the University of Toronto who has spent decades studying folate and infant health, this could be a problem. She explained that in animal models, it has been shown that folate can make changes to the genes that are transcribed during development. And while similar data have not been done on humans, she said “if you’re not getting any benefit from those high levels, it would be prudent to cut back given the current status…(because) if there’s no benefit, there’s only a risk.”

From a regulatory point-of-view, she says there’s nothing stopping the industry from changing the amount of folic acid in the supplements. She suggested that the industry’s reluctance to modify the dose in prenatal supplements is probably due to inertia and the fact that “with nutrition you’re always fighting against the more is better philosophy.”

In the meantime, what should women do? In their 2015 clinical practice guidelines, the Society of Obstetrics and Gynecologists recommended a multivitamin containing 400 to 1000 micrograms of folic acid. But currently, there are no prenatal vitamins available with less than 1000. Hence, Dr. O’Connor’s recommendation is “do not use the prenatal, just use a regular multi-vitamin and maybe add a little iron.” Furthermore, she added “care must be taken to ensure vitamin A intakes do not exceed 3,000 mcg retinol activity equivalents (RAE) or 10,000 IU during pregnancy.”

Alas, it’s a classic story, you try to fix one problem, but in doing so, you create another. Hopefully prenatal supplements will be adjusted soon, but in the meantime, prudent folic acid intakes are probably a good idea.