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.

What is Nutrigenomics

What Is The Truth About Personalized Nutrition Testing? – Part 2

Author: Dr. Stephen Chaney

 

nutrigenomicsWhen the human genome was sequenced in 2003, many of us in the scientific community thought we were on the verge of a revolution in human health and longevity. We would soon be able to tell individuals their risk of developing various diseases.

Even better, we would be able to tell them the kind of diet and supplementation they needed to avoid those diseases. We would be able to personalize our nutritional recommendation for every individual based on their genome – something called nutrigenomics.

How naive we were! It has turned out to be much more complicated to design personalized nutrition recommendations based on someone’s genome than we ever imagined.

 

What Is Nutrigenomics?

what is nutrigenomicsAs a Professor at the University of North Carolina I specialized in cancer drug development for over 30 years. Over the last decade of my career a field called pharmacogenomics became widely accepted in the field of cancer drug development. In simple terms, pharmacogenomics looks at how an individual’s genes influence the effectiveness and side effects of drugs.

Because of pharmacogenomics, drugs today are being approved to target cancers for people whose cancer cells have a particular genetic makeup. These drugs would not have been approved a decade ago because if you test them on cancer in the general population, they have little or no effectiveness. They only work on a subset of people who have a form of cancer with a specific genetic makeup.

In principle, nutrigenomics is the same principle. You’ve heard for years that we all have unique nutritional needs. Now we are starting to learn why. It’s because we all have unique variations in our genetic makeup. These genetic mutations increase our risk of certain diseases, and they increase our needs for certain nutrients.

For example, mutations in the MTHFR gene increase the risk of certain birth defects, and supplementation with folic acid is particularly important for reducing birth defects in that population group.

Similarly, mutations in the vitamin D receptor, the VDR gene, interfere with vitamin D absorption from foods and are associated with a condition known as “vitamin D-resistant rickets.” Babies born with this genetic defect require mega doses of vitamin D for normal bone formation.

These are the best-established examples of gene mutations that affect nutritional needs. Many more gene-nutrient interactions have been proposed, but they have not been validated by follow-up experiments.

The situation is similar when we look at gene mutations associated with metabolic responses such as fat and carbohydrate metabolism, obesity, insulin resistance and type 2 diabetes. There are a few gene mutations that have strong associations with obesity and diabetes. Many more gene-metabolism interactions have been proposed, but the data are weak and inconsistent.

 

The Promise Of Nutrigenomics

 

promise of nutrigenomicsNow that you understand what nutrigenomics is and have some background information about it, let’s look at the promise of nutrigenomics. One promise of nutrigenomics is personalized supplement programs.

We all have different nutritional needs. Wouldn’t it be wonderful if someone could analyze your genome and provide you with a personalized supplement program that precisely fits your genetically determined nutritional requirements?

There are companies that offer such personalized supplement programs. Are they providing you with something of value or is their testing bogus? Are their supplements worthless?

Another promise of nutrigenomics is personalized diet advice. Some people seem to do better on low-fat diets. Other people do best on low-carb diets. Saturated fats and red meats may be more problematic for some individuals than for others. Wouldn’t it be wonderful if someone could analyze your genome and provide you with a personalized diet program – one that allows you to lose weight easily and gain vibrant health.

There are companies that will analyze your genome and tell you whether you are more likely to lose weight and be healthier on a low-fat or low-carbohydrate diet. Is their testing accurate or is it bogus? Are they providing you with useful information, or is their diet advice worthless?

 

The Problem With Nutrigenomics

 

the truth signThe short answer to the questions I posed in the previous section is that personalized supplement and diet programs are on the horizon, but we are not there yet. Companies promising you personalized nutrition programs based on DNA tests are misleading you. They quote a few studies supporting the tests they run and ignore the many studies showing their tests are worthless.

In case you think that is just my opinion, let me quote from some recent reviews on the current status of nutrigenomics.

For example, a review (C Murgia and MM Adamski, Nutrients, 366, 2017) published in 2017 concluded: “The potential applications to nutrition of this invaluable tool were apparent since the genome was mapped. The first articles discussing nutrigenomics and nutrigenetics were published less than a year after the first draft of the human DNA sequence was made available…However, fifteen years and hundreds of publications later, the gap between the experimental and epidemiologic evidence and health practice is not yet closed.”

thumbs down symbol“The [complexity] of the genotype information is not the only factor that complicates this translation into practice. The discovery of other levels of control, including epigenetics [modifications of DNA that affect gene expression] and the intestinal microbiome, are other complicating factors. While the science of nutritional genomics continues to demonstrate potential individual responses to nutrition, the complex nature of gene, nutrition and health interactions continues to provide a challenge for healthcare professionals to analyze, interpret and apply to patient recommendations.”

Another review (M Gaussch-Ferre et al, Advances in Nutrition, 9: 128-135, 2018 ) published in 2018 concluded: “Overall, the scientific evidence supporting the dissemination of genomic information for nutrigenomic purposes remains sparse. Therefore, additional knowledge needs to be generated…”

In short, the experts are saying we still don’t know enough to predict the best diets or the best supplements based on genetic information alone. Why is that? Why is it so complicated? In part, it can be explained by a term called penetrance. Penetrance simply means that the same gene mutation can have different effects in different people. In some people, its effects may be barely noticeable. In other people its effects may be debilitating.

 

What Is The Truth About Personalized Nutrition Testing?

 

Penetrance is not just a word. It’s a concept. What causes differences in genetic penetrance? Here are the most likely explanations.

  • Human genetics is very complex. There are some gene mutations, such as those causing cystic fibrosis and sickle cell anemia, that can cause a disease by themselves. Most gene mutations, however, simply predispose to a disease or metabolic disturbance and are highly influenced by the activity of other genes. That’s because the products of gene expression form intricate regulatory and metabolic networks. When a single gene is mutated, it interacts with many other genes in the network. And, that network is different for each of us.
  • Many common diseases are polygenic. That includes disease like heart disease, diabetes, and most cancers. Simply put, that means that they are not caused by a single gene mutation. They are caused by the cumulative effect of many mutations, each of which has a small effect on disease risk. The same appears to be true for mutations that influence carbohydrate and fat metabolism and affect nutrient requirements.
  • The outcome of gene mutations is strongly influenced by our diet, lifestyle, and environment. For example, a common mutation in a gene called FTO predisposes to obesity. However, the effect of this mutation on obesity is strongest when it is coupled with inactivity and foods of high caloric density (translation: junk foods and fast foods instead of fresh fruits and vegetables). Simply put, that means most of us are genetically predisposed to obesity if we follow the American lifestyle, but obesity is not inevitable.
  • Epigenetics has an important influence on gene expression. When I was a graduate student, we believed our genetic destiny was solely determined by our DNA sequence. That was still the prevailing viewpoint when the human genome project was initiated. We thought that once we had our complete DNA sequence, we would know everything we needed to know about our genetic destiny.

nutrigenomics microbiomeHow short sighted we were! It turns out that our DNA can be modified in multiple ways. These modifications do not change the DNA sequence, but they can have major effects on gene expression. They can turn genes on or turn them off. More importantly, we have come to learn that these DNA modifications can be influenced by our diet, lifestyle, and exposure to environmental pollutants.

This is the science we call epigenetics. We have gone from believing we have a genome (DNA sequence) that is invariant and controls our genetic destiny to understanding that we also have an “epigenome” (modifications to our DNA) that is strongly influenced by our diet, lifestyle, and environment and can change day-to-day.

  • Our microbiome has an important influence on our health and nutritional status. Simply put, the term microbiome refers to our intestinal microbes. Our intestinal bacteria are incredibly diverse. Each of us has about 1,000 distinct species of bacteria in our intestines.

Current evidence suggests these intestinal bacteria influence our immune system, inflammation and auto-immune diseases, brain function and mood, and our predisposition to weight gain – and this may just be the tip of the iceberg.

More importantly, our microbiome is influenced by our diet. For example, vegetarians and meat eaters have entirely different microbiomes. Furthermore, the effect of diet on our microbiome is transitory. If you change your diet, the species of bacteria in your microbiome will completely change in a few weeks.

Finally, our microbiome also influences our nutritional requirements. For example, some species of intestinal bacteria are the major source of biotin and vitamin K2 for all of us and the major source of vitamin B12 for vegans. Intestinal bacteria may also contribute to our supply of folic acid and thiamine. Other intestinal bacteria inactivate and/or remove some vitamins from the intestine for their own use. Thus, the species of bacteria that populate our intestines can influence our nutritional requirements.

Now that you know the complexity of gene interactions you understand why we are not ready to rely on DNA tests yet. We don’t yet know enough to design a simple DNA test to predict our unique nutritional needs. That science is at least 10-20 years in the future. Companies that tell you otherwise are lying to you.

 

My Recommendations for Supplements and Foods

Here are my recommendations for how to decide which foods or supplements you should eat:

  • steve chaneyThink of DNA testing as only the first step in the process of learning which foods and supplements are best for you. Since DNA testing is not definitive by itself, I wouldn’t recommend spending thousands of dollars on a DNA test.
  • Next, start with diets that we know are healthy long-term. As I discussed in my book, “Slaying The Food Myths,” any primarily plant-based diet ranging from vegan to Mediterranean and DASH diets is likely to be healthy long-term. If you find you need a low carb diet, I recommend the low-carb version of the Mediterranean diet.
  • Don’t eliminate plant food groups like fruits, whole grains, or legumes from your diet unless you have an objective reason to do so (more about that below).
  • Learn to listen to your body. Keep track of the foods and/or supplements you eat and how they make you feel.
  • In terms of listening to your body, start with your digestive system. I have vegan friends who experience constant gas and bloating and think of it as a badge of honor. I have keto friends who experience constant constipation and think of it as a badge of honor. Neither is correct. That is just their body telling them the diet they are eating is not right for them. Here is the process I recommend:
  • Start by trying the various plant-based diets for 4 to 6 weeks until you find the one that works best for you. For example, when I tried that approach it became clear that a vegan diet was not for me. I discovered I do much better on a semi-vegetarian diet.
  • If you are still experiencing digestive issues, start paying more attention to the foods you are eating. If you keep a log of the foods you eat and when you experience digestive issues for a few weeks, you will likely be able to identify foods that are problematic for you. Once you have done that, eliminate them from your diet for a few weeks and then go back and do a food challenge test where you add that food back to your diet to confirm that it is a problem for you.
  • If all this fails, I recommend an elimination diet or FODMAP diet to identify foods to avoid (You can find instructions for both on the internet). [Note: Skin tests are notoriously unreliable, but they may give you some clues about foods to avoid that you could confirm with a food challenge.]
  • Finally, if digestive issues persist, you should make an appointment with your doctor.
  • Also, pay attention to blood sugar control following the same approach I outlined for digestive issues.
  • Symptoms of high blood sugar are fatigue, thirst, headache, trouble concentrating, and frequent urination.
  • Symptoms of low blood sugar are hunger, shakiness, anxiety, irritability, feeling lightheaded, and sleepiness.
  • Biomarkers of disease, like LDL cholesterol, HDL cholesterol, triglycerides, c-reactive protein (a measure of inflammation), and HbA1c (a measure of blood sugar control), can be useful indicators of whether a diet or supplement is right for you. However, you should interpret improvements in disease biomarkers with caution because they can be misleading when you have been following a diet or supplement program for a short time.

Any diet that results in rapid weight loss will improve disease biomarkers in the short term. Similarly, some supplement programs give a transitory improvement in disease biomarkers. It is only when a diet or supplement program has been followed for 5, 10, or 20 years that disease biomarkers become truly reliable indicators of the success or failure of that diet or supplement program.

  • Finally, feelings of well-being, energy, mood, and clarity of thinking are subjective and highly susceptible to the placebo effect. They are the least reliable indicators of the success or failure of a food or supplement program.

 

The Bottom Line

 

Nutrigenomics is defined as the interaction between our genetic makeup and our diet. How far have we advanced in the science of nutrigenomics? Can a simple DNA test provide us with useful information?

For example, we all have different nutritional needs. Wouldn’t it be wonderful if someone could analyze your genome and provide you with a personalized supplement program that precisely fits your genetically determined nutritional requirements?

There are companies that offer such personalized supplement programs. Are they providing you with something of value or is their testing bogus? Are their supplements worthless?

There are companies that will analyze your genome and tell you whether you are more likely to lose weight and be healthier on a low-fat or low-carbohydrate diet. Is their testing accurate or is it bogus? Are they providing you with useful information, or is their diet advice worthless?

Two recent reviews have surveyed the nutrigenomic literature (all published clinical studies) and have concluded that we still don’t know enough to predict the best diets or the best supplements based on genetic information alone. Why is that? It is because:

  • Human genetics is very complex.
  • Many common diseases are polygenic (caused by the cumulative effect of many mutations).
  • The effect of gene mutations on our health and wellbeing is strongly influenced by our diet, lifestyle, and environment.
  • Epigenetics has an important influence on gene expression.
  • Our microbiome has an important influence on our health and nutritional status.

For more details and my personal recommendations on how to determine the best diet and supplement program for you, 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.

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