Does Poverty Affect Nutritional Status?

How Can We Improve Nutrition In Disadvantaged Communities?

Calcium FoodsRecently there has been increased focus on health disparities in disadvantaged communities. In our discussions of the cause of these health disparities, two questions seem to be ignored.

1. Does poverty play a role in poor nutrition?

2. Does poor nutrition play a role in the health disparities we see in disadvantaged communities?

The study (K Marshall et al, PLoS One 15(7):e0235042) I discuss in this week’s “Health Tips From The Professor” attempts to address both of these questions.

Before, I start, let me put this study into context.

  • Osteoporosis is a major health problem in this country. Over 2 million osteoporosis-related fractures occur each year, and they cost our health care system over 19 billion dollars a year. Even worse, for many Americans these osteoporosis-related fractures often cause:
    • A permanent reduction in quality of life.
    • Immobility, which can lead to premature death.
  • Inadequate calcium and vitamin D intakes increase the risk of osteoporosis.

While most studies simply report calcium and vitamin D intakes for the general population, this study breaks them down according to ethnicity and income levels. The results were revealing.

How Was The Study Done?

Clinical StudyThis study drew on data from the 2007-2010 and 2013-2014 National Health and Nutrition Examination Surveys (NHANES). These surveys are conducted by the National Center for Health Statistics, which is part of the CDC. They are designed to assess the health and nutritional status of adults and children in the United States and are used to produce health statistics for the nation.

The NHANES interview includes demographic, socioeconomic, dietary, and health-related questions. The examination component consists of medical, dental, and physiological measurements, as well as laboratory tests administered by highly trained medical personnel. All participants visit a physician. Dietary interviews and body measurements are included for everyone.

This study measured calcium intake, vitamin D intake, and osteoporosis for adults 50 and older. The data were separated by gender, ethnic group and income level. Four different measures of poverty were used. For purposes of simplicity, I will only use one of them, income beneath $20,000, for this article.

Does Poverty Affect Nutritional Status?

The Effect of Ethnicity And Gender On Calcium And Vitamin D Intake: 

FriendsWhen the authors looked at the effect of ethnicity and gender on calcium and vitamin D intake, in people aged 50 and older the results were (Note: I am using the same ethnic nomenclature used in the article):

Hispanics:

    • 66% (75% for women and 56% for men) were getting inadequate calcium intake.
    • 47% (47% for women and 47% for men) were getting inadequate vitamin D intake.

Non-Hispanic Blacks:

    • 75% (83% for women and 64% for men) were getting inadequate calcium intake.
    • 53% (51% for women and 54% for men) were getting inadequate vitamin D intake.

Non-Hispanic Whites:

    • 60% (64% for women and 49% for men) were getting inadequate calcium intake.
    • 33% (30% for women and 37% for men) were getting inadequate vitamin D intake.

For simplicity, we can generalize these data by saying:

Gender:

    • Women are more likely to be calcium-deficient than men.
    • Men are more likely to be vitamin D-deficient than women.

Ethnicity: For both genders and for both calcium and vitamin D:

    • The rank order for deficiency is Non-Hispanic Blacks > Hispanics > Non-Hispanic Whites.

The Effect Of Poverty On Calcium Intake, Vitamin D Intake, And Osteoporosis:

PovertyWhen looking at the effect of poverty, the authors asked to what extent poverty (defined as income below $20,000/year) increased the risk of calcium and vitamin D deficiency in adults over 50. Here is a summary of the data

Hispanics:

    • For both Hispanic women and Hispanic men, poverty had little effect on the risk of calcium and vitamin D deficiency.

Non-Hispanic Blacks:

    • For Non-Hispanic Black women, poverty had little effect on the risk of calcium deficiency, and vitamin D deficiency.
    • For Non-Hispanic Black men, poverty increased the risk of both calcium and vitamin D deficiency by 32%.

Non-Hispanic Whites:

    • For Non-Hispanic White women, poverty had little effect on the risk of calcium deficiency but increased the risk of vitamin D deficiency by 30%.
    • For Non-Hispanic White men, poverty increased the risk of both calcium deficiency and vitamin D deficiency by 18%.

For simplicity, we can generalize these data by saying:

    • Poverty increased the risk of both calcium and vitamin D deficiency for Non-Hispanic Black men, Non-Hispanic White women, and Non-Hispanic White men.

Other statistics of interest:

  • The SNAP program (formerly known as Food Stamps) had little effect on calcium and vitamin D intake. There are probably two reasons for this:
    • In the words of the authors, “While the SNAP program has been shown to decrease levels of food insecurity, the quality of the food consumed by SNAP participants does not meet the standards for a healthy diet.” In other words, the SNAP program ensures that participants have enough to eat, but SNAP participants are just as likely to prefer junk and convenience foods as the rest of the American population. The SNAP program provides no incentive to eat healthy foods.
    • We also need to remember that dairy foods are a major source of calcium and vitamin D in the American diet and that Hispanics and Non-Hispanic Blacks are more likely to be lactose-intolerant than the rest of the American population. There are other sources of calcium and vitamin D in the American diet. But without some nutrition education, most Americans are unaware of what they are.
  • An increased risk of osteoporosis was found in Non-Hispanic Black men, and Non-Hispanic Whites with incomes below $20,000/year.
    • This increased risk of osteoporosis was seen primarily for the individuals in each group who were deficient in calcium and vitamin D. There were other factors involved, but I will focus primarily on the effect of poverty on calcium and vitamin D intake in the discussion below.

How Can We Improve Nutrition In Disadvantaged Communities?

Questioning WomanLet’s start with the two questions I posed at the beginning of this article:

1. Does poverty play a role in poor nutrition?

2. Does poor nutrition play a role in the health disparities we see in disadvantaged communities?

In terms of calcium intake, vitamin D intake, and the risk of osteoporosis, the answer to both questions appears to be, “Yes”. So, the question becomes, “What can we do?”

It is when we start to ask what we can do to increase calcium and vitamin D intake and decreased the risk of osteoporosis in disadvantaged communities that we realize the complexity of the problem. There are no easy answers. Let’s look at some of the possibilities.

[Note: I am focusing on what we can do to prevent osteoporosis, not to detect or treat osteoporosis. The solutions for those issues would be slightly different.]

1. We could increase funding for SNAP. That would increase the quantity of food available for low income families, but, as noted above, would do little to improve the quality of the food eaten.

2. We could improve access to health care in disadvantaged communities. But unless physicians started asking their patients what they eat and start recommending a calcium and vitamin D supplement when appropriate, this would also have little impact on diet quality.

3. We could improve nutrition education. A colleague of mine in the UNC School of Public Health ran a successful program of nutrition education through churches and community centers in disadvantaged communities for many years. The program taught people how to eat healthy on a limited budget. Her program improved the health of many people in disadvantaged communities.

However, the program was funded through grants. When she retired, federal and state money to support the program eventually dried up. The program she started is a model for what we should be doing.

4. The authors suggested food fortification as a solution. In essence, they were suggesting that junk and convenience foods be fortified with calcium and vitamin D. That might help, but I don’t think it is a good idea.

If we want to improve the overall health of disadvantaged communities, we need to find ways to replace junk and convenience foods with healthier foods. Adding a few extra nutrients to unhealthy foods does not make them healthy.

5. The authors also said that a calcium and vitamin D supplement would be a cheap and convenient way to eliminate calcium and vitamin D deficiencies. Unfortunately, supplements are currently not included in the SNAP program. Unless that is changed, even inexpensive supplements are a difficult choice for families below the poverty line.

As I said at the beginning of this section, there are no easy answers. It is easy to identify the problem. It would be easy to throw money at the problem. But finding workable solutions that could make a real difference are hard to identify.

Yes, we should make sure every American has enough to eat. Yes, we should make sure every American has access to health care. But, if we really want to improve the health of our disadvantaged communities, we also need to:

  • Change the focus of our health care system from treatment of disease to prevention of disease.
  • Train doctors to ask their patients what they eat and to instruct their patients how simple changes in diet could dramatically improve their health.
  • Provide basic nutrition education to disadvantaged communities at places where they gather, like churches and community centers. This would cover topics like eating healthy, shopping healthy on a limited budget, and cooking healthy.

We don’t necessarily need another massive federal program. But those of us with the knowledge could each volunteer to share that knowledge in disadvantaged communities.

  • Cover basic supplements, like multivitamins, calcium and vitamin D supplements, and omega-3 supplements in food assistance programs like SNAP.

The Bottom Line

Osteoporosis is a major health problem in this country. Over 2 million osteoporosis-related fractures occur each year, and they cost our health care system over 19 billion dollars a year. Even worse, for many Americans these osteoporosis-related fractures often cause:

  • A permanent reduction in quality of life.
  • Immobility, which can lead to premature death.

We know that inadequate calcium and vitamin D intakes increase the risk of osteoporosis. But most studies simply report calcium and vitamin D intakes for the general population. At the beginning of this article, I posed two questions.

  1.  Does poverty play a role in poor nutrition?

2. Does poor nutrition play a role in the health disparities we see in disadvantaged communities?

A recent study looked at the effect of gender, ethnicity and income levels on calcium intake, vitamin D intake, and the risk of developing osteoporosis. The results of this study shed some light on those two questions.

When looking at the effect of gender and ethnicity on the risk of inadequate calcium and vitamin D intake, the study found:

  • Women are more likely to be calcium-deficient than men.
  • Men are more likely to be vitamin D-deficient than women.
  • For both genders and for both calcium and vitamin D, the rank order for deficiency is Non-Hispanic Blacks > Hispanics > Non-Hispanic Whites. [Note: Note: I am using the same ethnic nomenclature used in the study.]
  • Poverty (defined as incomes below $25,000/year) significantly increased the risk of both calcium and vitamin D deficiency for Non-Hispanic Black men, Non-Hispanic White women, and Non-Hispanic White men.
  • An increased risk of osteoporosis was also found in Non-Hispanic Black men, and Non-Hispanic White men and women with incomes below $20,000/year.
  • This increased risk of osteoporosis was seen primarily for the individuals in each group who were deficient in calcium and vitamin D.

In short, this study suggests that the answer to both questions I posed at the beginning of the article is, “Yes”.

For more information and a discussion of what we could do to correct this health disparity in disadvantaged communities, read the article above.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease.

Does Maternal Vitamin D Affect Childhood ADHD?

Can ADHD Be Prevented?

vitamin dIf you are pregnant, or of childbearing age, should you be supplementing with vitamin D? Increasingly, the answer appears to be yes.

1) Based on blood 25-hydroxy vitamin D levels (considered the most accurate marker of vitamin D status):

    • 8-11% of pregnant women in the US are deficient in vitamin D (<30 nmol/L).
    • 25% of pregnant women have insufficient vitamin D status (30-49 nmol/L).

In short, that means around 1/3 of pregnant women in the US have insufficient or deficient levels of vitamin D. The effect of inadequate vitamin D during pregnancy is not just an academic question.

2) The Cochrane Collaboration (considered the gold standard for evidence-based medicine) has recently concluded that supplementation with vitamin D reduces the risk of significant complications during pregnancy.

3) Another recent study found that inadequate vitamin D status during pregnancy delayed several neurodevelopmental milestones in early childhood, including gross motor skills, fine motor skills, and social development.

If neurodevelopmental milestones are affected, what about ADHD? Here the evidence is not as clear. Some studies have concluded that vitamin D deficiency during pregnancy increases the risk of ADHD in the offspring. Other studies have concluded there is no effect of vitamin D deficiency on ADHD.

Why the discrepancy between studies?

  • Most of the previous studies have been small. Simply put, there were too few children in the study to make statistically reliable conclusions.
  • Most of the studies measured maternal 25-hydroxyvitamin D levels in the third trimester or in chord blood at birth. However, it is during early pregnancy that critical steps in the development of the nervous system take place.

Thus, there is a critical need for larger studies that measure maternal vitamin D status in the first trimester of pregnancy. This study (M Sucksdorff et al, Journal of the American Academy of Child & Adolescent Psychiatry, 2020, in press) was designed to fill that need.

How Was The Study Done?

Clinical StudyThis study compared 1,067 Finnish children born between 1998 and 1999 who were subsequently diagnosed with ADHD and 1,067 matched controls without ADHD. There were several reasons for choosing this experimental group.

  • Finland is among the northernmost European countries, so sun exposure during the winter is significantly less than for the United States and most other European countries. This time period also preceded the universal supplementation with vitamin D for pregnant women that was instituted in 2004.

Consequently, maternal 25-hydroxyvitamin D levels were significantly lower than in most other countries. This means that a significant percentage of pregnant women were deficient in vitamin D, something not seen in most other studies. For example:

    • 49% of pregnant women in Finland were deficient in vitamin D (25-hydoxyvitamin D <30 nmol/L) compared to 8-11% in the United States.
    • 33% of pregnant women in Finland had insufficient vitamin D status (25-hydroxyvitamin D 30-49.9 nmol/L) compared to 25% in the United States.
  • Finland, like many European countries, keeps detailed health records on its citizens. For example:
    • The Finnish Prenatal Study collected data, including maternal 25-hydroxyvitamin D levels during the first trimester), for all live births between 1991 and 2005.
    • The Care Register for Health Care recorded, among other things, all diagnoses of ADHD through 2011.

Thus, this study was ideally positioned to compare maternal 25-hydroxyvitamin D levels during the first trimester of pregnancy with a subsequent diagnosis of ADHD in the offspring. The long-term follow-up was important to this study because the average age of ADHD diagnosis was 7 years (range = 2-14 years).

Does Maternal Vitamin D Affect Childhood ADHD?

Child With ADHDThe answer to this question appears to be a clear, yes.

If you divide maternal vitamin D levels into quintiles:

  • Offspring of mothers in the lowest vitamin D quintile (25-hydroxyvitamin D of 7.5-21.9 nmol/L) were 53% more likely to develop ADHD than offspring of mothers in the highest vitamin D quintile (49.5-132.5 nmol/L).

When you divide maternal vitamin D levels by the standard designations of deficient (<30 nmol/L), insufficient (30-49.9 nmol/L), and sufficient (≥50 nmol/L):

  • Offspring of mothers who were deficient in vitamin D were 34% more likely to develop ADHD than children of mothers with sufficient vitamin D status.

The authors concluded: “This is the first population-based study to demonstrate an association between low maternal vitamin D during the first trimester of pregnancy and an elevated risk for ADHD diagnosis in offspring. If these findings are replicated, they may have public health implications for vitamin D supplementation and perhaps changing lifestyle behaviors during pregnancy to ensure optimal maternal vitamin D levels.”

Can ADHD Be Prevented?

Child Raising HandI realize that this is an emotionally charged title. If you have a child with ADHD, the last thing I want is for you to feel guilty about something you may not have done. So, let me start by acknowledging that there are genetic and environmental risk factors for ADHD that you cannot control. That means you could have done everything right during pregnancy and still have a child who develops ADHD.

Having said that, let’s examine things that can be done to reduce the risk of giving birth to a child who will develop ADHD, starting with vitamin D. There are two aspects of this study that are important to keep in mind.

#1: The increased risk of giving birth to a child who develops ADHD was only seen for women who were vitamin D deficient. While vitamin D deficiency is only found in 8-11% of pregnant mothers in the United States, that is an average number. It is more useful to ask who is most likely to be vitamin D deficient in this country. For example:

  • Fatty fish and vitamin D-fortified dairy products are the most important food sources of vitamin D. Fatty fish are not everyone’s favorite and may be too expensive for those on a tight budget. Many people are lactose intolerant or avoid milk for other reasons. If you are not eating these foods, you may not be getting enough vitamin D from your diet. This is particularly true for vegans.
  • If you have darker colored skin, you may have trouble making enough vitamin D from sunlight. If you are also lactose intolerant, you are in double trouble with respect to vitamin D sufficiency.
  • Obesity affects the distribution of vitamin D in the body. So, if you are overweight, you may have low 25-hydroxyvitamin D levels in your blood.
  • The vitamin D RDA for pregnant and lactating women is 600 IU, but many multivitamin and prenatal supplements only provide 400 IU. If you are pregnant or of childbearing age, it is a good idea to look for a multivitamin or prenatal supplement that provides at least 600 IU, especially if you are in one of the high risk groups listed above.
  • Some experts recommend 2,000 to 4,000 IU of supplemental vitamin D. I would not recommend exceeding that amount without discussing it with your health care provider first.
  • Finally, for reasons we do not understand, some people have a difficult time converting vitamin D to the active 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D in their bodies. If you are pregnant or of childbearing age, it is a good idea to have your blood 25-hydroxyvitamin D levels determined and discuss with your health care provider how much vitamin D you should be taking. Many people need more than 600 IU to reach vitamin D sufficiency status.

#2: Maternal vitamin D deficiency has a relatively small effect (34%) on the risk of the offspring developing ADHD. That means assuring adequate vitamin D status during pregnancy should be part of a holistic approach for reducing ADHD risk. Other factors to consider are:

  • Low maternal folate and omega-3 status.
  • Smoking, drug, and alcohol use.
  • Obesity.
  • Sodas and highly processed foods.

Alone, each of these factors has a small and uncertain influence on the risk of your child developing ADHD. Together, they may play a significant role in determining your child’s risk of developing ADHD.

In closing, there are three take-home lessons I want to leave you with:

1) The first is that there is no “magic bullet”. There is no single action you can take during pregnancy that will dramatically reduce your risk of giving birth to a child who will develop ADHD. Improving your vitamin D, folate, and omega-3 status; avoiding cigarettes, drugs, and alcohol; achieving a healthy weight; and eating a healthy diet are all part of a holistic approach for reducing the risk of your child developing ADHD.

2) The second is that we should not think of these actions solely in terms of reducing ADHD risk. Each of these actions will lead to a healthier pregnancy and a healthier child in many other ways.

3) Finally, if you have a child with ADHD and would like to reduce the symptoms without drugs, I recommend this article.

The Bottom Line

A recent study looked at the correlation between maternal vitamin D status during the first trimester of pregnancy and the risk of ADHD in the offspring. The study found:

  • Offspring of mothers who were deficient in vitamin D were 34% more likely to develop ADHD than children of mothers with sufficient vitamin D status.

The authors concluded: “This is the first population-based study to demonstrate an association between low maternal vitamin D during the first trimester of pregnancy and an elevated risk for ADHD diagnosis in offspring. If these findings are replicated, they may have public health implications for vitamin D supplementation and perhaps changing lifestyle behaviors during pregnancy to ensure optimal maternal vitamin D levels.”

In the article above I discuss what this study means for you and other factors that increase the risk of giving birth to a child who will develop ADHD.

For more details read the article above.

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease.

 

Does Vitamin D Prevent Type 1 Diabetes?

Does Genetics Influence Supplementation Benefits?

diabetesThe cause of type 1 diabetes is a mystery. If you go to an authoritarian source like the Mayo Clinic, you will discover that:

  • Type 1 diabetes is an autoimmune disease that selectively attacks the insulin-producing islet cells of the pancreas.
  • Certain genetic variants predispose individuals to type 1 diabetes.
  • The autoimmune response may be triggered by a viral infection or other unknown environmental factors in genetically susceptible individuals.
  • The incidence of type 1 diabetes increases as you travel away from the equator, which suggests that vitamin D may be involved.

The idea that vitamin D may be involved is an important concept because it suggests that vitamin D supplementation might reduce the risk of developing type 1 diabetes. This idea was reinforced by a Finnish study (E Hyponnen et al, Lancet, 358: 1500-1503, 2001) published in 2001 showing the vitamin D supplementation of newborn infants reduced the incidence of type 1 diabetes at age 1.

However, subsequent studies in other parts of the world have had mixed results. Some have confirmed the results of the Finnish study. Others have come up empty.

Similarly, some studies have shown a correlation between low 25-hydroxyvitamin D levels in the blood and the development of type 1 diabetes in children, while other studies have found no correlation.

Why the discrepancy between studies? Some of the differences can be explained by differences in the populations studied or differences in study design. But what if there were another variable that none of the previous studies has considered?

The study (JM Norris et al, Diabetes, 67: 146-154, 2018) I review this week describes just such a variable. The authors of the study hypothesized that the association between 25-hydroxyvitamin D levels and the risk of developing type 1 diabetes is influenced by mutations that affect the way vitamin D works in the body. Previous studies have not taken these mutations into account. If the author’s hypothesis is true, it might explain why these studies have produced conflicting results.

In this article, I will answer 3 questions:

  • Does vitamin D prevent type 1 diabetes?
  • If so, is supplementation with vitamin D important?
  • Who will benefit most from vitamin D supplementation?

But, before I answer those questions, I should begin by providing some background. I will start by reviewing the how diet, increased need, disease, and genetics influence the likelihood that we will benefit from supplementation. Then I will review vitamin D metabolism.

Does Genetics Influence Supplementation Benefits?

need for supplementsThe reason so many studies find no benefit from supplementation is that they are asking the wrong question. They are asking “Does supplementation benefit everyone?” That is an unrealistic expectation.

I have proposed a much more realistic model (shown on the left) for when we should expect supplementation to be beneficial. Simply put, we should ask:

  • Is the diet inadequate with respect to the nutrient that is being studied?
  • Is there an increased need for that nutrient because of age, gender, activity level, or environment?
  • Is there a genetic mutation that affects the metabolism or need for that nutrient?
  • Is there an underlying disease state that affects the need for that nutrient?

When clinical studies are designed without taking this paradigm into account, they are doomed to fail. Let me give you some specific examples.

  • The Heart Outcomes Prevention Evaluation study concluded supplementation with folate and other B vitamins did not reduce heart disease risk. The problem was that 70% of the people in the study were getting adequate amounts of folate from their diet at the beginning of the study. For those individuals not getting enough folate in their diet, B vitamin supplementation decreased their risk of heart disease by 15%. This is an example of poor diet influencing the need for supplementation.

The other three examples come from studies on the effect of vitamin E supplementation on heart disease that I summarized in an article in “Health Tips From The Professor” a few years ago. Here is a brief synopsis.

  • The Women’s Health Study concluded that vitamin E did not decrease heart disease risk in the general population. However, the study also found that in women over 65 (who are at high risk of heart disease), vitamin E supplementation decreased major cardiovascular events and cardiovascular deaths by 25%. This is an example of increased need because of age and gender influencing the need for supplementation.
  • The Women’s Antioxidant Cardiovascular Study” concluded that vitamin E did not decrease heart disease risk in the general population. However, when they looked at women who already had cardiovascular disease at the beginning of the study, vitamin E supplementation decreased risk of heart attack, stroke, and cardiovascular death by 23%. This is an example of an underlying disease affecting the need for supplementation.
  • The HOPE study concluded that vitamin E did not decrease heart disease risk in the general population. However, when they looked at individuals with a mutation that increases the risk of heart disease, vitamin E supplementation significantly decreased their risk of developing heart disease. This is an example of genetics affecting the need for supplementation.

These are just a few of many examples. When you ask whether supplementation benefits everyone, the answer is often no. However, when you look at people with inadequate diet, increased need, underlying disease, and/or genetic predisposition, the answer is often yes.

This background sets the stage for the current study. Of course, to understand the author’s hypothesis that mutations in genes involved in vitamin D metabolism might influence the effect of vitamin D on the risk of developing type 1 diabetes, you need to know a little about vitamin D metabolism.

Biochemistry 101: Vitamin D Metabolism

Vitamin D MetabolismWhen sunlight strikes a metabolite of cholesterol in our skin, it is converted to a precursor that spontaneously isomerizes to form vitamin D3. Because this series of reactions is usually not sufficient to provide all the vitamin D3 our bodies require, we also need to get vitamin D3 from diet and supplementation.

However, vitamin D3 is not active by itself. It first needs to be converted to 25-hydroxyvitamin D by our liver and then to the active 1,25-dihydroxyvitamin D. 1,25-dihydroxyvitamin D is an important hormone that regulates many cells in our body.

Some of the 1,25-dihydroxyvitamin D is synthesized by our kidneys and released into the bloodstream. This 1,25-dihyroxyvitamin D binds to vitamin D receptors on the surface of many cells and initiates regulatory pathways that affect metabolism inside the cell.

Other cells take up 25-hydroxyvitamin D and convert it to 1,25-dihydroxyvitamin D themselves. In these cells both the synthesis and regulatory effects of 1,25-dihydroxyvitamin D occur entirely inside the cell.

In both cases, it is 1,25-dihydroxyvitamin D that regulates cellular metabolism. The only difference is the way this regulation is accomplished.

There are two additional points that are relevant to this study.

  • The efficiency of conversion of vitamin D to 25-hydroxyvitamin D varies from person to person.
    • Thus, blood levels of 25-hydroxyvitamin D are considered a more reliable measure of vitamin D status than dietary intake of vitamin D or sun exposure.
    • Blood levels of 25-hydroxyvitamin D levels ≥50 nmol/L are considered optimal, while levels of 30 to <50 nmol/L are considered suboptimal, and levels <30 nmol/L are considered deficient.
  • 1,25-dihydroxyvitamin D binds to the vitamin D receptor on immune cells. This initiates a series of reactions that decrease the risk of autoimmune responses by our immune system.

How Was This Study Done?

Clinical StudyThis study was called TEDDY (The Environmental Determinants Of Type 1 Diabetes in the Young). Between September 2004 and February 2010, 424,788 newborn infants from 6 medical centers in Colorado, Georgia, Washington, Finland, Germany, and Sweden were screened for genes that predispose to type 1 diabetes.

The investigators identified 21,589 high-risk infants, and 8,676 of them were enrolled in this study before age 4 months. Clinic visits for the children occurred every 3 months between 3 and 48 months of age and every 6 months thereafter.

  • A DNA sample was taken at the time they entered the study and analyzed for mutations in genes involved in vitamin D metabolism.
  • 25-hydroxy vitamin D levels were obtained at each office visit. Because some studies have suggested the vitamin D status during the first year of life is important, the data were analyzed in two ways.
    1. An average of all 25-hydroxyvitamin D levels (referred to as “childhood 25-hydroxyvitamin D levels”).
    1. An average of 25-hydroxyvitamin D levels during the first 12 months (referred to as “early infancy 25-hydroxyvitamin D levels”).
  • Serum autoantibodies to pancreatic islet cells were measured at each office visit as a measure of an autoimmune attack on those cells. Persistent autoimmune response was defined as positive autoantibodies on two consecutive office visits.

While this study did not directly measure type 1 diabetes, children with an autoimmune response to their pancreatic islet cells are highly likely to develop type 1 diabetes. Thus, for purposes of simplicity I will refer to “risk of developing type 1 diabetes” rather than “persistent autoimmune response” in describing these results.

    1. 418 children developed persistent autoantibodies to their pancreatic islet cells during the study. The onset of this autoimmune response ranged from 2 months to 72 months with an average of 21 months.
    1. These children were compared to 3 matched controls from their medical center who did not develop an autoimmune response.

This study was remarkable for two reasons:

1) It was much larger than previous studies. This gave it greater power to detect an effect of vitamin D status on the risk of developing type 1 diabetes.

2) This was the first study to ask whether mutations in genes controlling the metabolism of vitamin D influenced the effect of vitamin D on the risk of developing type 1 diabetes.

Does Vitamin D Prevent Type 1 Diabetes?

Vitamin DThe study compared the risk of developing type 1 diabetes in children whose 25-hydroxyvitamin D levels were optimal (≥50 nmol/L) to children whose 25-hydroxyvitamin D levels were suboptimal (30 to <50 nmol/L). The results were:

  • Optimal vitamin D status during childhood was associated with a 31% decrease in the risk of developing type 1 diabetes.
  • Optimal vitamin D status during early infancy (first 12 months) was associated with a 40% decrease in the risk of developing type 1 diabetes.

In other words, having optimal vitamin D status significantly reduces the likelihood of developing of type 1 diabetes in childhood.

  • 25-hydroxyvitamin D levels >75 nmol/L provided no additional benefit.

In other words, you need sufficient vitamin D, but higher levels provide no additional benefit.

  • They tested 5 genes involved in vitamin D metabolism to see if they influenced the effect of vitamin D on the risk of developing type 1 diabetes. Only the VDR (vitamin D receptor) gene had any influence.
    • When the VDR gene was fully functional, optimal vitamin D status had no effect on the risk of developing type 1 diabetes. This means that even suboptimal (30 to <50 nmol/L) levels of 25-hydroxyvitamin D were sufficient to prevent type 1 diabetes when the vitamin D receptor was fully functional.
    • Only 9% of the children in this study were vitamin D deficient (<30 nmol/L 25-hydroxyvitamin D). Presumably, these children would be at high risk of developing type 1 diabetes even with a fully functional VDR gene. However, there were not enough children in that category to test this hypothesis.
  • When they looked at children with mutations in the VDR gene:
    • Optimal vitamin D status during childhood was associated with a 59% decrease in the risk of developing type 1 diabetes.
    • Optimal vitamin D status during early infancy (first 12 months) was associated with a 67% decrease in the risk of developing type 1 diabetes.

In short, the need for optimal vitamin D levels to reduce the risk of developing type 1 diabetes is only seen in children with a mutation in the VDR (vitamin D receptor) gene.

  • This is a clear example of genetics affecting the need for a nutrient.
    • For children with a fully functional VDR gene, even 30-50 nmol/L 25-hydroxyvitamin D was sufficient to reduce the risk of developing type 1 diabetes.
    • However, children with mutations in the VDR gene required ≥50 nmol/L 25-hydroxyvitamin D to reduce their risk of developing type 1 diabetes.
  • This is also an example of genetics affecting the need for supplementation with vitamin D.
    • 42% of the children in this study had suboptimal levels of 25-hydroxyvitamin D. Those who also have a mutation in the VDR gene would require supplementation to bring their 25-hydroxyvitamin D up to the optimal level to reduce their risk of developing type 1 diabetes.
    • Other studies have estimated that up to 61% of children in the US may have suboptimal 25-hydroxyvitamin D levels.

What Does This Study Mean For You?

Questioning WomanLet’s start with the three questions I proposed at the beginning of this article.

1) Does vitamin D prevent type 1 diabetes? Based on this study, the answer appears to be a clear yes. However, this is the first study of this kind. We need more studies that into account the effect of mutations in the VDR gene.

2) If so, is supplementation with vitamin D important? If we think in terms of supplementation with RDA levels of vitamin D or sufficient vitamin D to bring 25-hydroxyvitamin D into the optimal range, the answer is also a clear yes. However, there is no evidence from this study that higher doses of vitamin D provide additional benefits.

3) Who will benefit most from vitamin D supplementation? Based on this study, the children who will benefit the most from vitamin D supplementation are those who have a suboptimal vitamin D status and have a mutation in the VDR (vitamin D receptor) gene. To put this into perspective:

    • Up to 60% of children and adults in this country have suboptimal vitamin D levels.
    • The percentage of suboptimal vitamin D levels is highest for people who are obese, have pigmented skin, are institutionalized (eg, elderly in nursing homes), and/or live far from the equator.
    • Supplementation with a multivitamin containing the RDA for vitamin D reduces the risk of having suboptimal vitamin D status by 2.5 to 5-fold depending on the person’s ethnicity.
    • This study may be just the tip of the iceberg. The vitamin D receptor is also found on many other cells that control important biological functions.

Finally, if you are a parent or parent-to-be, you probably have several questions. Here are the ones I have New Parentsanticipated:

#1: Is my child at risk for developing type 1 diabetes? If you or a close family member has type 1 diabetes, you can assume your child is genetically predisposed to developing type 1 diabetes. Other factors that increase your child’s risk of developing type 1 diabetes are obesity, non-White ethnicity, and geographical location far from the equator.

#2: Should I have my baby tested for genetic predisposition to type 1 diabetes? That is not currently recommended. Just be aware of the risk factors listed above.

#3: Should I have my baby tested for VDR mutations? That is unnecessary. If your child has a VDR mutation, they just need sufficient vitamin D, not mega doses of vitamin D. And there are lots of other reasons for making sure your child gets sufficient vitamin D.

#4: How much vitamin D should my child be getting? The recommendation is 400 IU up to age 1 and 600 IU over age 1.

#5: Should I give my child vitamin D supplements? It is a good idea. For children over age 1, I recommend a multivitamin supplying 600 IU of vitamin D.

For infants, the American Association of Pediatrics recommends 400 IU vitamin D drops, regardless of whether the infants are breast or formula fed. That is because studies during the first year of life show that less than one-fifth of all infants get the recommended 400 IU/d from any source, and fewer than one out of 10 breast-fed infants meet the requirement – even if the mother is getting adequate vitamin D in their diet.

One Caution: I do not recommend exceeding 400 IU for infants or 600 IU for children unless directed by your health care provider. In terms of the risk of developing type 1 diabetes, your child needs sufficient vitamin D, and more is not better.

#6: Should I have my child tested for 25-hydroxyvitamin D levels? That is not done routinely at the present time. However, if your child has one or more of the risk factors listed above, it is a conversation you should have with your health care provider.

The Bottom Line

While it is widely accepted that vitamin D helps reduce the risk of developing type 1 diabetes in childhood, that has been difficult to prove. Clinical studies have provided conflicting results. The authors of a recent study postulated that the discrepancies between studies may have arisen because the studies neglected the effect of mutations in genes controlling vitamin D metabolism which may affect the ability of vitamin D to reduce the risk of developing type 1 diabetes.

This study found that:

1) Infants and children with optimal vitamin D status (25-hydroxyvitamin D levels ≥50 nmol/L) were 31-40% less likely to develop type 1 diabetes than children with suboptimal vitamin D status (25-hydroxyvitamin D = 30 to <50 nmol/L).

2) However, the effect of vitamin D on the risk of developing type 1 diabetes was only seen in children with one or more mutations in the VDR (vitamin D receptor) gene. To interpret this observation, you need to know that:

    • Type 1 diabetes is caused by an autoimmune attack on the pancreatic islet cells that release insulin.
    • 1,25-dihydroxyvitamin D promotes immune tolerance and decreases the risk of autoimmune responses.
    • 1,25-dihydroxyvitamin D exerts this effect by binding to the vitamin D receptor on the surface of immune cells.

3) Thus, mutations in the VDR gene modify the effect of vitamin D on the risk of developing type 1 diabetes. Specifically:

    • When the VDR gene is fully active, even suboptimal levels of vitamin D appear to be sufficient to prevent the development of type 1 diabetes in childhood.
    • However, when the VDR gene has mutations that reduce its activity, suboptimal levels of vitamin D no longer prevent type 1 diabetes. Optimal levels of vitamin D are required to reduce the risk of developing type 1 diabetes.

This is an example of genetics increasing the need for a nutrient (vitamin D) and increasing the need for supplementation to make sure that optimal levels of that nutrient are achieved.

While this study focused on the effect of vitamin D on the development of type 1 diabetes, this may just be the tip of the iceberg. The vitamin D receptor is also found on many other cells that control important biological functions.

For more details, read the article above. You will probably want to read the section “What Does This Mean For You?”, including my recommendations for parents of young children

These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease.

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