Dr. Steve Chaney

Could Mom’s Stress Affect Her Baby’s Health?

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How Can You Minimize Stress During Pregnancy?

StressIf you are pregnant, the advice you see on the internet can be overwhelming. There are so many things you “must do” and so many things you “must avoid” if you want a healthy baby. It’s enough to stress you out.

As if that weren’t bad enough, we are probably living through the most stressful period in recent memory. So, the last thing you want to hear is that your stress during pregnancy can affect the health of your baby.

Before I go any further, let me make it clear that the studies I will discuss in this issue of “Health Tips From the Professor” are intriguing, but they are preliminary. I don’t want to add to your stress.

Let me start by reviewing the literature:

  • Several studies suggest that stress during pregnancy is associated with preterm birth, low birthweight, and infant mortality.
  • Other studies suggest that stress during pregnancy is associated with suboptimal cognitive development, hyperactivity, and asthma in the offspring.

The big question, of course, is how a mom’s stress during pregnancy can affect the health of her child months or years later. One hypothesis is that stress affects the mom’s gut bacteria, and those gut bacteria are passed along to the child as he or she passes through the birth canal.

We know that stress can affect your gut bacteria, but can it affect your child’s gut bacteria? Studies in mice suggest it can. Today I will discuss the first large clinical study (AK Aatsinki et al, Pyschoneuroendocrinology, 119 (2020) 104754) designed to evaluate that hypothesis in humans.

How Was This Study Done?

Clinical StudyThis study was an offshoot of an ongoing FinnBrain Cohort Project, which aims to study the influence of stress exposures during pregnancy on later childhood development and health outcomes. This particular study was designed to investigate the role of chronic stress during pregnancy on the population of gut bacteria in infants. There were 399 mothers and their babies who completed this study.

All Participants in the FinnBrain Project:

  • Filled out self-reported prenatal questionnaires at gestational weeks 14, 24, and 34. These questionnaires provided background information about the health, weight, age, and education level of the moms, as well as whether they were taking antidepression medications during their pregnancy.
  • Were also asked about breast feeding 2.5 months after giving birth.
  • Duration of gestation, birth weight, and method of delivery information were obtained from Finland’s National Institute for Health and Welfare.

Participants in this study:

  • Were evaluated for depression and anxiety symptoms three times during pregnancy and at 3 months after giving birth. It should be noted that the questionnaires used to evaluate depression and anxiety symptoms did not measure the stressors (events causing the stress). Instead they were measuring the mom’s response to those stressors.
  • Cortisol levels were measured at gestational week 24 as another measure of the mother’s stress level.
  • Fecal samples were obtained from the offspring at the age of 2.5 months and analyzed for the population of gut bacteria.

Could Mom’s Stress Affect Her Baby’s Health?

Bad BacteriaThe results of this study were intriguing:

Infants born to mothers who experienced high levels of stress (such as depression and/or anxiety) during pregnancy had an increased abundance of potentially pathogenic gut bacteria such as:

  • Serratia, Haemophilus, Citrobacter, and Campylobacter from the Proteobacteria group of bacteria.
  • Veillonella and Finegoldia from the Firmicutes group of bacteria.

In addition, infants born to mothers with elevated cortisol levels (another measure of stress) had decreased abundance of potentially health promoting gut bacteria such as Lactobacillus.

In contrast:

  • Infants born to mothers who experienced low levels of stress had increased levels of potentially health promoting gut bacteria, such as Akkermansia.
  • Infants born to mothers with low cortisol levels had an increased abundance of Lactobacillus in their gut.

In short:

  • High levels of stress in the mother during pregnancy are associated with an increased abundance of unhealthy bacteria in their baby’s intestine.
  • Low levels of stress in the mother during pregnancy are associated with an increased abundance of healthy bacteria in their baby’s intestine.

The authors concluded:

“The observed fecal bacteria signature in the infants with exposure to chronic maternal stress, such as increased abundance of potentially inflammatory bacteria from the Proteobacteria group of bacteria, warrant future follow-up of these children, since similar alterations of fecal bacteria have previously been associated with adverse health outcomes such as asthma in children.

The results of this study describe only associations, yet corroborate certain interesting findings reported in earlier literature and offer hypotheses for future mechanistic studies.”

How Can You Minimize Stress During Pregnancy?

Simply put, this study shows that chronic stress during pregnancy increases populations of gut bacteria in the newborn that are associated with adverse health outcomes in children. More studies are needed to confirm and understand this observation, but it raises an issue that is often ignored.

Pregnancy can be a stressful time, especially if you are a first-time mom. Plus, we are living in the most stressful time any of us can remember. So, this study is particularly relevant today.

However, let’s put this into perspective. It’s not the stress in our lives that harms us. It is how we respond to the stress. This study did not measure stress, per se. It measured depression, anxiety, and cortisol levels associated with the stress.

Some of the women in this study had very low levels of all three. It wasn’t that they led stress-free lives. They simply coped better with stress. So, the real question isn’t how to minimize stress. It’s how to better cope with stress. Here are some suggestions.

1) Take time to relax. What you do with this time will be different for each of you. Think about what kind of activity relaxes you the most. Here are some suggestions.

    • Meditation or prayer.
    • Yoga or Tai chi.
    • Watching a comedy.
    • Listening to your favorite music.

2) Make time for hobbies. Again, these would be different for each of you. They should be something that you enjoy and engages your mind. Examples include:

    • Reading.
    • Creating your favorite art. It could be painting, pottery, or knitting, for example.
    • Playing your favorite sport such as golf or tennis.
    • Doing puzzles.
    • Playing cards or board games.
    • Watching a movie.

3) Exercise on a regular basis. Exercise produces endorphins that elevate your mood. It’s even better if you are exercising outdoors so you can enjoy nature or listening to your favorite music while you exercise.

4) Relax your muscles. This is particularly important after you have exercised. Examples include:

    • Do some stretching exercises.
    • Take a luxurious hot bath.
    • Set a regular time to go to bed and get a good night’s sleep.
    • Get a massage.

5) Eat a healthy diet. Studies have shown that people who eat lots of junk and processed foods tend to be depressed and anxious. Aim for a whole food diet with lots of fruits and vegetables. That kind of diet is best for your baby as well.

6) Try deep breathing exercises.

7) Ask for support from your family members, especially if they are stressors in your life.

8) Talk with someone. Find a friend or family member who is willing to listen and support you.

In short, take care of yourself. Don’t let stress affect your health and the health of your baby.

The Bottom Line

Pregnancy can be a stressful time, especially if you are a first-time mom. Plus, we are living in the most stressful time any of us can remember. That is why a recent study is particularly relevant.

Simply put, the study showed that chronic stress during pregnancy increases populations of gut bacteria in the newborn that are associated with adverse health outcomes in children. More studies are needed to confirm and understand this observation, but it raises an issue that is often ignored.

However, let’s put it into perspective. It’s not the stress in our lives that harms us. It is how we respond to the stress. This study did not measure stress, per se. It measured depression, anxiety, and cortisol levels associated with the stress.

Some of the women in this study had very low levels of all three. It wasn’t that they led stress-free lives. They simply coped better with stress. So, the real question isn’t how to minimize stress. It’s how to better cope with stress.

For more details and a discussion on how to cope with stress, 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.

What Is The Truth About Eating Eggs And Heart Disease?

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Have The Dangers Of Eggs Been “Eggagerated”?

egg confusionIt’s no wonder you are confused about whether or not eggs are good for you. The advice you have been given about eggs over the years has been constantly changing.

Eggs are an affordable source of high-quality protein, iron, unsaturated fats, phospholipids like lecithin and choline, and carotenoids. That almost qualifies them as a health food. However, they are also a major source of cholesterol in the American diet. Back when we thought of dietary cholesterol was bad for us, that made eggs the enemy.

Then we discovered that dietary cholesterol has relatively little effect on blood cholesterol levels. It was obesity plus saturated fat and sugar in our diet that raised blood cholesterol levels and increased our risk of heart disease.

Then several studies reported that eggs did not increase our risk of heart disease. A study out of China even found that eggs decreased the risk of heart attack and hemorrhagic stroke. Suddenly, eggs became our best friend.

That only lasted a few years until a study from the United States reported that eggs increased your risk of heart disease, and a study from Europe reported that eggs increased your risk of hemorrhagic stroke. Eggfusion (egg confusion) reigned.

Most of these studies were large studies. They followed their participants for 5-10 years. Why were their results so confusing? A careful analysis of the studies shows that most of them suffered from three major weaknesses.

  • They only measured egg consumption at the beginning of the study. This fails to account for the fact that egg consumption has waxed and waned over the years as eggs have gone from enemy to friend and back to enemy.
  • They did not assess how the overall diet influences the effect of egg consumption on heart disease. If we believe the previous studies, eggs lower the risk of heart disease and hemorrhagic stroke in China and increase the risk of both in the United States and Europe. This suggests that overall diet is important, but this hypothesis has not been tested.
  • They also did not address the question of whether eggs, because of their cholesterol, might have a more adverse effect on heart disease in individuals who already have high blood cholesterol and have difficulty controlling their cholesterol levels.

That is why the study (JP Drouin-Chartier et al, British Medical Journal, 368:m513, 2020) I am reporting on today is so important. It is a huge study, much larger than any previous study on the topic. Plus, it was designed in such a way that it had none of the weaknesses of previous studies.

How Was The Study Done?

Clinical StudyThis study started by combining the data from three major clinical trials:

  • The first Nurse’s Health Study, which ran from 1980 to 2012,
  • The second Nurse’s Health Study, which ran from 1991-2013, and
  • The Health Professional’s Follow-Up Study, which ran from 1986-2012.

These studies combined enrolled 173,563 women and 42,055 men and followed them for an average of 32 years. All the participants were free of heart disease, type 2 diabetes, and cancer at the time they were enrolled. The design of these studies was extraordinary.

  • A detailed food frequency questionnaire was administered every 2-4 years. This allowed the investigators to calculate cumulative averages of all dietary variables, including egg intake. This assured that the effects of egg consumption and diet represented the participant’s diet over the 32-year duration of the study.
  • Participants also filled out questionnaires that captured information on disease diagnosis, disease risk factors, medicines taken, weight, and lifestyle characteristics every 2 years with follow-up rates >90%. This allowed the investigators to measure the onset of disease and medicine use for each participant during the study. More importantly, 32 years is long enough to measure the onset of diseases like heart disease, diabetes, and cancer – diseases that require decades to develop.
  • The endpoint of the study was “incident heart disease”, which the investigators defined as non-fatal heart attack, death from heart disease, and fatal and non-fatal stroke. During this study, 14,806 participants developed incident heart disease. This was a large enough number for a detailed statistical analysis of the data.
  • For example, statistical analysis showed that the participants with the highest egg intake also were more likely to be obese and more likely to consume red meat, bacon and other processed meats, refined grains, French fries, and sugar-sweetened beverages. These are what we refer to as “confounding variables” because they also increase the risk of heart disease and are likely to confound (confuse) the analysis. Therefore, the investigators statistically corrected the data on egg consumption for these confounding variables. Many previous studies did not have the data or statistical power to correct their egg consumption data for these confounding variables.

In short, this study was much larger, ran far longer, and was better designed that any of the previous studies on egg consumption and heart disease risk. However, the authors did not stop there. They also performed a meta-analysis of 28 previous studies with a total of 1,720,108 participants and 139,195 cardiovascular disease events.

The only weakness in this study is that only 2% of the participants ate more than one egg per day. Consequently, it cannot address the health consequences of eating more than one egg per day on a regular basis.

Before sharing the results of this study with you, I need to provide some background about how our bodies regulate blood cholesterol levels. So, let’s move on to my favorite topic, “Biochemistry 101”.

Biochemistry 101: Cholesterol Metabolism

ProfessorMost people think of cholesterol only as a bad thing – something that can kill us. Nothing could be further from the truth. In fact, cholesterol is essential for life.

  • Our body makes vitamin D and coenzyme Q10 from cholesterol.
  • Our body makes steroid hormones such as cortisol, estrogen, and testosterone from cholesterol.
  • Cholesterol is a vital component of the myelin sheath that coats our nerve cells.
  • And that is just the beginning.

Because cholesterol is essential, our body makes its own cholesterol and has an elegant control system that keeps our blood cholesterol levels right where they should be.

  • When we get lots of cholesterol from our diet, our body makes less and excretes any excess.
  • When we get little cholesterol from our diet, our body makes more and excretes less.

Unfortunately, many Americans muck up this elegant control system. There are several factors that can throw our body’s ability to regulate blood cholesterol levels out of whack, leading to elevated blood cholesterol levels and increased risk of heart disease. For example:

  • Obesity
  • Type 2 diabetes
  • Diets high in saturated fats
  • Diets high in sugar and refined carbohydrates
  • Genetics

And it’s not just elevated cholesterol that is the problem. These same factors are associated with inflammation, which also increases the risk of heart disease.

Of course, we can’t do anything about our genetics, but the other factors are under our control. Let’s keep that in mind as we look at the results of this study.

What Is The Truth About Eating Eggs And Heart Disease?

the truth signWhen the investigators looked at their combined data from the Nurse’s Health Studies and the Health Professional’s Study:

  • There was no difference in heart disease outcomes for participants consuming an average of one egg/day and participants consuming less than one egg/month.
  • When the investigators examined heart attack and stroke separately, there was no difference in either outcome for participants consuming an average of one egg/day and participants consuming less than one egg/month.
  • As mentioned above the participants who consumed the most eggs weighed more; were less physically active; were more likely to be current smokers; and were more likely to consume red meat, processed meats, refined grains, potatoes (think French fries and potato chips), full fat milk, and sugar-sweetened beverages.
    • Without correcting for these factors eating one egg/day resulted in a 10% increase in heart disease risk.
    • After correcting for these factors, eating one egg/day resulted in a 7% decrease in heart disease risk.
    • In both cases the differences were statistically non-significant. However, they were in line with the previous studies mentioned above.

When they looked at the data generated by their meta-analysis of 28 studies:

  • There was no association between heart disease risk and egg consumption.
    • In Asian countries where the diet was primarily unrefined, plant-based foods, egg consumption decreased heart disease risk.
    • In people with type 2 diabetes, egg consumption increased heart disease risk.

The authors concluded “…moderate egg consumption (up to one egg/day) is not associated with cardiovascular disease risk overall, and is associated with potentially lower cardiovascular disease risk in Asian populations.”

The authors also noted that their data did not allow them to evaluate the effect of consuming more than one egg/day.

Have The Dangers Of Eggs Been “Eggagerated”?

are eggs good for youThis study clears up a lot of confusion about egg consumption and heart disease risk. The problem is that the scientific and medical communities have been looking for a “one size fits all” recommendation about egg consumption. This study shows us that the reality is much more complicated. Let me describe my interpretation of the data.

I think the results of this and previous studies are best described by the phrase, “Eggs are a healthy part of a healthy diet”. Here is what I mean by that.

  • If you are consuming a primarily plant-based diet, your body is fully able to regulate your blood cholesterol levels. Then, you can reap the full benefits of the egg, namely the protein, iron, unsaturated fats, lecithin, choline, and carotenoids it provides. Under these conditions, eating up to one egg/day reduces your risk of heart disease.
  • If you are consuming a diet that contains primarily chicken or fish and unprocessed plant foods, egg consumption is neutral. It neither increases nor decreases your risk of heart disease.
  • If you are consuming a diet that contains sugar-sweetened beverages, red and processed meats, high fat dairy products, refined grains, and junk foods (ie, the typical American diet), your body is no longer able to regulate blood cholesterol levels well. Now the cholesterol content of eggs becomes an issue and consuming one egg/day slightly increases your risk of heart disease.
  • If you are overweight and have developed type 2 diabetes, your body has become insulin resistant. This also interferes with your body’s ability to regulate blood cholesterol levels. In this situation, consuming one egg/day also increases your risk of heart disease.

The caveat is, of course, that these conclusions are based averages, and none of us are average.

The Bottom Line

You are probably aware that the effect of egg consumption on heart disease risk is controversial. Some studies report that egg consumption has no effect on heart disease risk. Other studies report egg consumption decreases heart disease risk. Still other studies report that egg consumption increases heart disease risk. No wonder you are confused.

A recent study has cleared up much of the confusion. This was not just another study. This study was much larger, ran far longer, and was better designed that any of the previous studies.

If you look at this and previous studies, it becomes clear that the effect of egg consumption on heart disease risk is strongly influenced by your overall diet and lifestyle.

  • If you are consuming a primarily plant-based diet, your body is fully able to regulate your blood cholesterol levels. Then, you can reap the full benefits of the egg, namely the protein, iron, unsaturated fats, lecithin, choline, and carotenoids it provides. Under these conditions, eating up to one egg/day reduces your risk of heart disease.
  • If you are consuming a diet that contains primarily chicken or fish and unprocessed plant foods, egg consumption is neutral. It neither increases nor decreases your risk of heart disease.
  • If you are consuming a diet that contains sugar-sweetened beverages, red and processed meats, high fat dairy products, refined grains, and junk foods (ie, the typical American diet), your body is no longer able to regulate blood cholesterol levels well. Now the cholesterol content of eggs becomes an issue and consuming one egg/day slightly increases your risk of heart disease.
  • If you are overweight and have developed type 2 diabetes, your body has become insulin resistant. This also interferes with your body’s ability to regulate blood cholesterol levels. In this situation, consuming one egg/day also increases your risk of heart disease.

In short, eggs are a healthy part of a healthy diet.

For more details, read the article above. You may also want to read the section “Biochemistry 101: Cholesterol Metabolism” to gain a better understanding of the mechanism behind these statements.

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

Can Vitamin C Prevent Heart Disease?

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Where Should I Get My Vitamin C?

vitamin CThe vitamin C controversy continues. Some people call vitamin C a “miracle” nutrient. Others consider it little more than “fairy dust”. What is the truth?

Let’s look at the effect of vitamin C on heart disease risk as an example of why it is so difficult to resolve questions like this.

Association studies are ideal for measuring long-term effects of nutrient consumption on health outcomes. These studies have consistently found an inverse association between dietary vitamin C and plasma vitamin C levels with the risk of heart disease. Simply put, the more vitamin C from dietary sources, the lower the risk of heart disease.

However, association studies do not prove cause and effect. The primary reason for this is that association studies are complicated by “confounding variables”. For example, most vitamin C in the diet comes from fruits and vegetables. So, the question arises, “Is it the vitamin C in fruits and vegetables that is responsible for the decreased heart disease risk, or is it the fiber that is also present in fruits and vegetables?” Previous studies have not been designed to answer this question.

Placebo-controlled clinical trials solve the confounding variable issue because they involve supplementation with pure vitamin C or a placebo. There is only a single variable. However, placebo-controlled clinical trials only last for a short time. That means they can measure biological markers that may affect heart disease risk but seldom last long enough to directly measure the effect of vitamin C on heart disease risk.

For example, previous studies have shown that high-dose (500 to 4,000 mg/day) supplementation with vitamin C improves the function of the endothelial lining of our blood cells and reduces blood pressure. These are biological markers that might be expected to reduce heart disease risk.

However, heart disease takes decades to develop. No studies of vitamin C supplementation have lasted long enough to show an actual decrease in heart disease outcomes.

In today’s issue of “Health Tips From The Professor” I would like to address three questions:

1) Does dietary vitamin C reduce heart disease risk?

2) How much of the risk reduction is due to the fiber content of fruits and vegetables rather than their vitamin C content?

3) Does supplementation with vitamin C reduce heart disease risk?

I will focus on a recent study (N Martin-Calvo and MA Martinez-Gonzalez, Nutrients, 9: 954, 2017, doi.org/10.3390/nu909054) that was designed to answer these questions.

How Was The Study Done?

Heart Health StudyThis study was an offshoot of an ongoing Spanish research program called Seguimiento Universidad de Navarra (SUN) follow-up study. This program is following graduates of the University of Navarra to gauge the effect of diet and lifestyle on health outcomes.

Health, lifestyle, and diet information is collected when graduates enroll in the program and by mailed questionnaires every two years thereafter.

Graduates who were enrolled in the SUN program in 2014 or earlier were invited to participate in this vitamin C and heart disease study.

  • Vitamin C intake from diet and from supplements was assessed from the dietary analysis.
  • A diagnosis of heart disease was obtained from the Health questionnaire and confirmed by physician follow-up.
  • Deaths due to heart disease were obtained from the Spanish National Death Index cross-referenced to participants in the study and were confirmed by participants next of kin, work associates, or postal authorities.

The study excluded:

  • Participants with pre-existing heart disease at the beginning of the study.
  • Participants who were younger than 40 at the beginning of the study.
  • Participants with either very high or very low vitamin C intake.

That left 13,421 participants who were young (average age = 42), at a healthy weight (average BMI = 24), healthy, and taking few medications.

Can Vitamin C Prevent Heart Disease?

Healthy HeartThe 13,421 participants in this study were followed for an average of 11 years.

They were divided into three groups based on their vitamin C intake.

  • Group 1 averaged 148 mg/day.
  • Group 2 averaged 257 mg/day.
  • Group 3 averaged 445 mg/day.

There are two noteworthy observations about their vitamin C intake:

  • None of the groups were vitamin C deficient. All three groups were getting well above the RDA for vitamin C (75 mg/day for women and 90 mg/day for men).
  • Most of the vitamin C came from fruits and vegetables in the diet. The group with the highest vitamin C intake (445 mg/day) only averaged about 10 mg/day from supplements.

The results of the study were intriguing. When the investigators compared the group with the highest vitamin C intake to the group with the lowest vitamin C intake:

  • Vitamin C significantly decreased both the risk of developing heart disease and the risk of dying from heart disease.
    • Statistically adjusting the data for age, gender, weight, lifestyle, and medicine use did not affect the outcome.
    • Statistically adjusting the data for fiber from sources other than fruits and vegetables did not affect the outcome.
    • Statistically adjusting the data for adherence to a healthy diet (the Mediterranean diet) did not affect the outcome.

However, when the data were statistically adjusted for total fiber (including fiber from fruits and vegetables) the high fiberresults painted a slightly different picture. With this adjustment:

  • Vitamin C decreased the risk of developing heart disease by 26%, but this decrease was not statistically significant.
  • Vitamin C decreased the risk of dying from heart disease by 70%, and this decrease was highly significant.

This was the first study to consider the relative importance of vitamin C from fruits and vegetables and fiber from fruits and vegetables on heart disease outcomes and the results were interesting. Here are the important conclusions.

1) Both the fiber and the vitamin C from fruits and vegetables contributed to a decreased risk of developing heart disease. This study was unable to separate their contributions.

Of course, it is important to note that this was a young, healthy population, none of whom were deficient in vitamin C. It would be interesting to repeat this study with an older, sicker population with a more restrictive diet.

2) Vitamin C from fruits and vegetables reduced the risk of dying from heart disease independent of the beneficial effects of fruit and vegetable fiber.

3) This study was not able to address the effect of vitamin C supplementation on heart disease risk. That is because the Spaniards supplement much less frequently than Americans and this study excluded anyone with unusually high vitamin C intake. The average supplemental vitamin C in the 3 groups ranged from 0.56 mg/day to 9.6 mg/day.

4) This study also emphasizes the importance of getting fiber from a variety of food sources. It showed that fiber from fruits and vegetables was more beneficial at reducing heart disease risk than fiber from other food sources. That means restrictive diets that eliminate fruits and/or vegetables may be bad for your heart.

Where Should I Get My Vitamin C?

Vegan FoodsThis study reinforces the importance of getting lots of fresh fruits and vegetables in your diet.

  • You could make a list of all the vitamin C-rich fruits and vegetables like citrus fruits, red & green peppers, broccoli, etc. and make sure you are including them in your diet.
  • You could total up the vitamin C in each food you eat and try to reach the 445 mg/day in the group with the highest vitamin C in this study.

However, it doesn’t have to be that complicated. If you eat a primarily plant-based diet, aim for 5-9 servings of fruits and vegetables a day, and “eat the rainbow” you will get plenty of vitamin C from your diet.

Also, don’t worry about whether the benefits of fruit and vegetable consumption come from their vitamin C or from their fiber. That’s the beauty of eating whole foods. You get both in the same package.

Of course, you are probably also wondering whether vitamin C supplementation will reduce your risk of heart disease. As I described earlier, there are lots of reasons for thinking that vitamin C supplementation might decrease heart disease risk.

  • Several studies show that higher vitamin C intake and higher vitamin C levels in the blood are associated with lower heart disease risk.
  • This study showed that vitamin C reduces the risk of dying from heart disease independent of fiber from fruits and vegetables and independent of an overall healthy diet. This suggests that vitamin C plays an independent role in reducing heart disease risk.
  • Placebo controlled clinical trials show that vitamin C supplementation reduces risk factors that contribute to heart disease.

However, none of these studies prove that vitamin C supplementation reduces heart disease risk. That requires placebo-controlled clinical trials measuring the effect of vitamin C supplementation on heart disease outcomes. Unfortunately, these studies are usually doomed to failure.

Chronic diseases like heart disease takes decades to develop. Placebo-controlled, randomized studies are almost never large enough or last long enough to show an effect of supplementation on chronic diseases.

The best we can say at present is that vitamin C supplementation along with a primarily plant-based diet with lots of colorful fruits and vegetables may reduce your risk of heart disease.

The Bottom Line

A recent study in Spain followed 13,421 healthy college graduates with an average age of 42 for 11 years and looked at the effect of vitamin C intake on the risk of developing heart disease and the risk of dying from heart disease.

This was the first study to consider the relative importance of vitamin C from fruits and vegetables and fiber from fruits and vegetables on heart disease outcomes and the results are intriguing. Here are the important conclusions.

1) Both the fiber and the vitamin C from fruits and vegetables contributed to a decreased risk of developing heart disease. This study was unable to separate their contributions.

Of course, it is important to note that this was a young, healthy population, none of whom were deficient in vitamin C. It would be interesting to repeat this study with an older, sicker population with a more restrictive die

2) Vitamin C from fruits and vegetables reduced the risk of dying from heart disease by 70%, and this effect was independent of the beneficial effects of fruit and vegetable fiber.

3) This study was not able to address the effect of vitamin C supplementation on heart disease risk. That is because the Spaniards supplement much less frequently than Americans and this study excluded anyone with unusually high vitamin C intake. The average supplemental vitamin C in the 3 groups ranged from 0.56 mg/day to 9.6 mg/day.

4) This study also emphasizes the importance of getting fiber from a variety of food sources. It showed that fiber from fruits and vegetables was more beneficial at reducing heart disease risk than fiber from other food sources. That means restrictive diets that eliminate fruits and/or vegetables may be bad for your heart.

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.

Is Stress Causing My Headaches?

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“It’s Summertime, and the Living Is…Stressful”

headacheIt’s hot out, the birds are chirping, the air is pretty still, and the rains are often torrential.  It’s summer and under normal circumstances things slow down as people take vacations or just go to sit at the beach or pool.  Normally, we would be singing that old favorite, “It’s summertime and the living is easy”.

But this year is different! This summer’s song could be, “It’s summertime and the living is stressful.

We’ve all been affected by COVID19 in some manner, life is more complicated for most of us, and stress-levels have increased for a lot of people. Since stress often causes headache pain, today’s newsletter is going to focus on relieving stress headaches.

Stress Can Tighten Your Muscles

Constant stress can tie your muscles into knots.   It is important to do things to relieve the stress that the current events are placing on your body.  Maybe you aren’t going to the gym, but you can go out for a long, fast walk.  You could even bring some light hand weights and be pumping your arms as you walk.  If you have access to a pool, swimming is a great way to get exercise without stressing the body – with social distancing, of course.

There are several muscles that cause headaches. Unfortunately, it’s rare that anyone in the medical field will check out muscles while looking for the source of headache pain.

Is Stress Causing My Headaches?

As I said above, chronic stress can cause your muscles to tighten, and tight muscles can cause headaches. I will discuss two of the main offenders today.

Treating Temporalis MuscleOne muscle that causes headaches is called the Temporalis.  This muscle is the shape of a fan and is at the temples of your skull, behind your eyes and above your ears.  It not only causes headaches. It also causes pain into your top teeth!

To treat your Temporalis muscle, take your three middle fingers and press on the muscle as shown in the picture to the left.

Find the tender point, only pressing enough to feel it, but not so much that you want to faint. Hold the pressure for a minute and then move your fingers slightly up and down, without sliding on your skin.

Release the pressure for about 15 seconds and repeat this sequence until the pain is gone.

Do this treatment on both sides of your skull.  Stay still on any “hot spots” as they are the actual spasm that is causing the problem. You’ll be surprised at how the pain and tenderness will diminish as you continue to do the whole treatment for just a few minutes.

Levator Scapulae MuscleAnother key headache muscle is the Levator Scapulae, a muscle that originates on your cervical vertebrae and inserts into your shoulder blade.  When this muscle is in spasm it will pull your cervical vertebrae to the side and down and press the bone into your spinal cord at the base of your brain.  

Looking at how the levator scapulae muscle attaches to the vertebrae in your neck will explain why it is an important cause of stress headaches.

The levator scapulae originates on the top four cervical vertebrae (see small box) and inserts into the top of your shoulder blade.  When the muscle contracts normally you lift up your shoulders. The nickname for this muscle is “the shrug muscle” because of its action.

However, when it gets tight it will pull the insertions at your neck to the side and down. This causes the bones to press into your spinal cord, right at the base of your brain, and you get a severe headache!

Fortunately, you can treat the levator scapulae muscle, release the tension on the cervical vertebrae, and by treating the muscles in the back of your neck that become involved as the vertebrae move, you can stop the headache. It usually takes a while, maybe even two days. I wish I could tell you it’s immediate, but the important thing is you can stop the pain.

If you have suffered from headaches and your doctor has tested you to be sure it isn’t something more serious, then you’ll be pleased with the results of the Julstro™ self-treatments.

Relief From Stress Headaches Caused By A Tight Levator Scapula Muscle

Let me take you through the treatment step by step.

Relaxing Levator Scapulae MuscleStep 1: Relaxing the Spasms in Your Shoulders 

 You start by relaxing the spasms in your shoulders. While it can be awkward at first, you can very effectively treat your levator scapulae muscle by using a ball and pressing into the corner of a wall.

Put the Julstro Perfect ball directly on the top of your shoulder. Then lean straight into the corner of a wall.

Move slightly until you feel the pressure being focused on the knot at the top of your shoulder.

This treatment is for both your levator scapulae muscle and your trapezius muscle.

Step 2: Treating Your Levator Scapulae Muscle. 

Once you have loosened up the spasms in your shoulders, continue working on the levator scapulae muscle. You can also treat both by squeezing them with your fingers. We’ll demonstrate by treating your right shoulder. Naturally, you can do the same treatment on the opposite shoulder.

Bend your left arm and support you elbow with your right hand. Put your left three middle fingers on your right Treating Levator Scapulae Muscle shoulder at the point where the shoulder and neck meet. It helps if you place it so your thumb and pointer finger are close to your neck with the middle finger being the working finger right on the junction, just a bit toward the back. Your four fingers should be crooked at each joint of the hand and your palm should be flat against your body.

Staying in the same spot, relax your arm with your elbow close to the middle of your chest. In this position you will probably have your middle finger directly on the spasm point. All the strength from this move is coming from your upper arm, not from your fingers. To do that you will simply make sure that your middle finger is on the sore spot and then pull your elbow down toward the floor. Your finger will be like a hook that presses into the spasm.

If you feel your fingers getting tired, you are using your hand to give strength and not your arm. Once you feel the difference, it will be easy to do again. After you have found the trigger point and you are adding pressure to it, continue pressing into the knot.

Treating Levator Scapulae Muscle 2Next, keep your hand in the same spot, still pressing on the knot. Take your thumb, flip over onto the front of your shoulder, and push it straight into the muscle. This will move your thumb to a place that will now cause you to be pinching the knot.

You’ll feel if you have it right. You should have a fairly thick piece of muscle between the middle finger and the thumb. You can inch your three middle fingers back a bit if you find you aren’t gripping the entire thickness of the muscle.

If all you are feeling is skin between your fingertips, go back and try again. When you know you have a thick piece of muscle, grip tightly and release. Do this four times for 15 seconds each time.

 

Step 3: Stretching the Muscles in Your Shoulder

Now that you have worked out the knots, you are ready to stretch your shoulder muscles. Rotate your head a bit Stretching Levator Scapulae Muscleso your ear is angled toward the front of your chest. By doing this you will be adding additional stretch to the trigger point and releasing it at the same time.

Finally, continue holding the muscle and move your head as shown. Hold this for 15 seconds and release the pressure. When you finish, release your grip and shake out your shoulders. Then do it again, three more times, holding each stretch for 15 seconds.

You will really feel a great deal of relief when you ease the tension in this muscle.  This process will become easy after you play with it for a while and get the hang of squeezing the ball of knots that are on the top of your shoulder.

Wishing you well,

Julie Donnelly 

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.

Should I Avoid Whole Grains?

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Will Whole Grains Kill Me?

Whole GrainsIt seems like just yesterday that health experts all agreed that whole grains were good for us. After all:

  • They are a good source of fiber, B vitamins, vitamin E, and the minerals magnesium, iron, zinc, manganese, and selenium.
  • Their fiber fills you up, so you are less likely to overeat. This helps with weight control.
  • Their fiber also supports the growth of friendly bacteria in your gut.

In fact, the USDA still recommends that half of the grains we eat should be whole grains. And, outside experts, not influenced by the food industry, feel this recommendation is too low. They feel most of the grains we eat should be whole grains. Foods made from refined grains should be considered as only occasional treats.

Then the low-carb craze came along. Diets like Paleo and Keto were telling you to avoid all grains, even whole grains. Even worse, Dr. Strangelove and his colleagues were telling you whole grains contained something called lectins that were bad for you. Suddenly, whole grains went from being heroes to being villains.

You are probably asking, “Should I avoid whole grains?” What is the truth? Perhaps the best way to resolve this debate is to ask, how healthy are people who consume whole grains for many years? This week I share a recent study (G Zong et al, Circulation, 133: 2370-2380, 2016) that answers that very question.

How Was The Study Done?

This study was a meta-analysis of 14 clinical trials that:

  • Enrolled a total of 786,076 participants.
  • Obtained a detailed diet history at baseline.
  • Followed the participants for an average of 15 years (range = 6-28 years).
  • Determined the effect of whole grain consumption on the risk of death from heart disease, cancer, and all causes.

Will Whole Grains Kill Me?

deadDr. Strangelove and his colleagues are claiming that whole grains cause inflammation, which increases your risk of heart disease and cancer. Heart disease and cancer are the leading causes of death in this country. In fact, according to the CDC, heart disease and cancer accounted for 44% of all deaths in the US in 2017.

Therefore, if Dr. Strangelove and his colleagues were correct, consumption of whole grains should increase the risk of deaths due to heart disease and cancer – and increase the risk of death due to all causes.

That is not what this study showed.

When the highest whole grain intake (5 servings/day) was compared with the lowest whole grain intake (0 servings/day), whole grain consumption reduced the risk of death from:

  • Heart disease by 18%.
  • Cancer by 12%.
  • All causes by 16%.

Furthermore, the effect of whole grains on mortality showed an inverse dose response. Simply put, the more thumbs upwhole grains people consumed, the lower the risk of deaths from heart disease, cancer, and all causes.

However, the dose response was not linear. Simply going from 0 servings of whole grains to one serving of whole grains reduced the risk of death from.

  • Heart disease by 9%.
  • Cancer by 5%.
  • All causes by 7%.

The authors concluded: “Whole grain consumption was inversely associated with mortality in a dose-response manner, and the association with cardiovascular mortality was particularly strong and robust. These observations endorse current dietary guidelines that recommend increasing whole grain intake to replace refined grains to facilitate long-term health and to help prevent premature death.”

The authors went on to say: “Low-carbohydrate diets that ignore the health benefits of whole grain foods should be adopted with caution because they have been linked to higher cardiovascular risk and mortality.”

Should I Avoid Whole Grains?

Question MarkAs for the original question, “Should I avoid whole grains?”, the answer appears to be a clear, “No”.

The strengths of this study include the large number of participants (786,076) and the demonstration of a clear dose-response relationship between whole grain intake and reduced mortality.

This study is also consistent with several other studies that show whole grain consumption is associated with a lower risk of heart disease, diabetes, cancer – and appears to lead to a longer, healthier life.

In short, it appears that Dr. Strangelove and the low-carb enthusiasts are wrong. Whole grains aren’t something to avoid. They reduce the risk of heart disease, diabetes, and cancer. And they reduce the risk of premature death. We should be eating more whole grains, not less.

However, the authors did point out that this study has some weaknesses:

  • It is an association study, which does not prove cause and effect.
  • Study participants who consumed more whole grains also tended to consume more fruits and vegetables – and less red meat, sodas, and highly processed foods.

However, I would argue the second point is a strength, not a weakness. We need to give up the idea that certain foods or food groups are “heroes” or “villains”. We know that primarily plant-based diets like the Mediterranean and DASH diets are incredibly healthy. Does it really matter how much of those health benefits come from whole grains and how much comes from fruits and vegetables?

The Bottom Line

Dr. Strangelove and low-carb enthusiasts have been telling us we should avoid all grains, including whole grains. Is that good advice?

If Dr. Strangelove and his colleagues were correct, consumption of whole grains should increase the risk of deaths due to the top two killer diseases, heart disease and cancer. Furthermore, because heart disease and cancer account for 44% of all deaths in this country, whole grain consumption should also increase the risk of death due to all causes.

A recent study showed the exact opposite. The study showed:

When the highest whole grain intake (5 servings/day) was compared with the lowest whole grain intake (0 servings/day), whole grain consumption reduced the risk of death from:

  • Heart disease by 18%.
  • Cancer by 12%.
  • All causes by 16%.

Furthermore, the effect of whole grains on mortality showed an inverse dose response. Simply put, the more whole grains people consumed, the lower the risk of deaths from heart disease, cancer, and all causes.

However, the dose response was not linear. Simply going from 0 servings of whole grains to one serving of whole grains reduced the risk of death from.

  • Heart disease by 9%.
  • Cancer by 5%.
  • All causes by 7%.

The authors concluded: “Whole grain consumption was inversely associated with mortality in a dose-response manner, and the association with cardiovascular mortality was particularly strong and robust. These observations endorse current dietary guidelines that recommend increasing whole grain intake to replace refined grains to facilitate long-term health and to help prevent premature death.”

The authors went on to say: “Low-carbohydrate diets that ignore the health benefits of whole grain foods should be adopted with caution because they have been linked to higher cardiovascular risk and mortality.”

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 Maternal Vitamin D Affect Childhood ADHD?

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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.

 

Can DNA Testing Help You Lose Weight?

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How Does DNA Testing Work Best?

Genetic TestingGenomics (DNA testing) is hot. You are being told that if you just knew your genes, you could lose weight successfully, be healthier, be happier, leap tall buildings in a single bound (Actually, I haven’t heard the last claim, but it’s about the only claim that genomics marketers haven’t made). Which of these claims are true, and which are just hot air?

The experts agree that the benefits of DNA testing have been greatly oversold. As I said in a recent article on DNA testing, the idea that genes control our destiny is no longer considered valid. There are 3 reasons for this. I will start with the scientific term for each and then give you the non-scientific explanation.

  • Penetrance simply means that the severity of most gene mutations is influenced by our genetic background. Simply put, the same mutation can have a significant effect in one individual and a trivial effect in another individual.
  • Epigenetics refers to modifications of the DNA that influence gene expression. These DNA modifications are, in turn, influenced by diet and lifestyle.
  • Microbiome refers our gut bacteria. In many cases, our microbiome has just as much influence on our health as our genes. And our microbiome is influenced by diet and lifestyle.

Now you know the complexity of DNA testing, it is easy to see why experts feel that it is premature to use DNA testing to predict the best diet for either weight loss or health.

As an example, one recent study used DNA testing to predict whether study participants were more likely to lose weight on a low-carb or low-fat diet. The participants were then randomly assigned to low-carb and low-fat diets. At the end of 12 months:

  • There was no significant difference in weight loss for those on low-fat and low-carb diets. This has been reported in multiple previous studies but is an inconvenient truth that most low-carb enthusiasts tend to ignore.
  • DNA testing offered no predictive value as to whether a low-carb or low-fat diet was more effective for weight loss.

However, DNA testing may have one benefit that is overlooked by many experts. What if the DNA test results motivated people to do better? After all, most diet advice is generic. People feel it may or may not apply to them. Does personalized diet advice based on their genetic makeup motivate people to stick with the diet better?

Some studies have suggested that people may follow personalized diet plans based on their DNA more faithfully. However, most of those studies have been short-term.

That is why I have chosen today’s study (J Horne et al, BMJ Nutrition, Prevention & Health, 2020) to discuss. It is a very well-designed study and it lasted for a full year.

How Was The Study Done?

Clinical StudyThis was an extremely well-designed study. In fact, it was so well designed that it probably needs the “Results are not typical” designation the FDA requires when some diet companies make claims about weight loss success. Here are the details:

  • The study participants were highly motivated, college educated, middle-aged (average age = 55), obese (average weight = 216 pounds) Caucasian women who had a positive attitude about their ability to change what they ate. In case you weren’t counting, there were four characteristics of this group that might be considered atypical for the average American.
  • The participants volunteered for a highly structured weight loss program called the “Group Lifestyle Balance”, or GLB, program.
    • Participants were given a detailed calorie-controlled nutrition plan at the beginning of the program.
    • They were asked to track their daily food and beverage intake for the first 2-3 months of the program.
    • In the second week of the program participants were educated on how to count and track calories and nutrients such as total fat or saturated fat.
    • There were weekly meetings with dietitians the first 3 months and monthly meetings for the remainder of the 12-week program to provide the guidance and support needed to stick with their nutrition plan.
  • The plan also incorporated a behavior change program called Theory of Planned Behavior (TPB) that evaluates and influences attitudes, subjective norms, and behavioral control that are key to behavior change. During the regular meetings:
    • The participants were informed about of the health benefits associated with a healthy lifestyle.
    • They were educated on positive mindsets and mindfulness.
    • They were taken through a stepwise, goal setting approach designed to positively impact behavioral change.

In short, this is a gold standard diet program that provided the nutritional support needed to stick with the diet program and the psychological support needed to change eating behavior. Unfortunately, this is also atypical. Very few diet programs provide this level of support.

Everyone in the study participated in this program. However, the participants were divided into two groups.

  • Both groups were advised to follow a standard calorie-controlled, moderately low-fat (25% of total calories) nutrition plan.
  • In addition, the second group was put on a plan that was either high protein or low saturated fat (<10% of total calories) based on their DNA test results.
  • The nutritional support was identical except that the second group was told that their nutrition plan was specific for them, based on their DNA analysis.
  • The dietary intake of both groups was assessed with a 3-day dietary recall (2 week days and 1 weekend day) at baseline (before the program began) and at 3, 6, and 12 months to assess the participants adherence to their diet plan.

Can DNA Testing Help You Lose Weight?

Happy woman on scaleI hate to disappoint you, but the short answer to this question, is no. Both groups lost the same amount of weight, which is not surprising considering the comprehensive nature of the diet program that both groups were enrolled in.

However, the group given advice based on their DNA test were more motivated to stick with their personalized nutrition goals. Specifically:

  • Long-term adherence to reductions in saturated fat intake was significantly greater in the group that was told their diet plan was personalized based on their DNA analysis.
    • The control group reduced their saturated fat intake by 12% at 3 months, but only by 4% at 6 months, and 2.5% at 12 months.
    • The group with the personalized diet plan reduced their saturated fat intake by 14% at 3 months, 18% at 6 months, and 22% at 12 months.
  • Long-term adherence to reductions in total fat intake was also significantly greater in the group that was told their diet plan was personalized based on their DNA analysis.
    • The control group reduced their total fat intake by 18% at 3 months, but only by 4% at 6 and 12 months.
    • The group with the personalized diet plan reduced their total fat intake by 11% at 3 months, 13% at 6 months, and 16% at 12 months.
    • It is important to remember that both groups had been advised to reduce their total fat intake to 25% of calories and had received nutritional and psychological support to achieve that goal. The only difference was that the second group had been told that advice was based on their DNA test.

The authors of the study concluded: “Weight management interventions guided by nutrigenomics can motivate long-term improvements in dietary fat intake above and beyond gold-standard population-based interventions.”

How Does DNA Testing Work Best?

DNA TestingThere remain significant concerns about the validity of personalized weight loss advice based on DNA testing. However, this and other studies suggest that DNA testing may provide one valuable asset for weight loss programs. It appears that people are more likely to stick with a program they believe has been personalized for them.

There are, however, several caveats to this conclusion.

  • Participants in this study received nutritional and psychological support throughout the 12-month program. We don’t know how well participants would have stuck with the program if they had not been continually reminded that the program had been personalized for them.
  • Participants in this study were well-educated, highly motivated, Caucasian women. We don’t know whether these results apply to men and to other ethnic and socioeconomic groups.
  • This study only looked at personalized diet advice based on DNA testing. Some studies suggest that other methods of diet personalization may also improve adherence.
  • Personalization can be misused to recommend unhealthy dietary changes. It is not enough to follow personalized diet advice. You also need to ask whether it is healthy dietary advice.

For example, DNA test results consistent with reduced carbohydrate intake are sometimes used to recommend unhealthy diets that eliminate one or more food groups rather than low-carb versions of healthy diets like the Mediterranean diet.

The Bottom Line

There remain significant concerns about the validity of personalized weight loss advice based on DNA testing. However, DNA testing may provide one valuable asset for weight loss programs. Some studies have suggested that people are more likely to stick with a program they believe has been personalized for them.

However, most of these studies have been short term. A recent study asked whether the improvement in motivation lasted for 12 months.

Two matched groups of well-educated, highly motivated women were enrolled in a “gold-standard” weight loss program that provided both nutritional and psychological support for 12 months.

Both groups were given a diet plan that restricted total calorie intake and advised reducing fat intake to 25% of total calories. However, based on their DNA test results one group was given a personalized diet plan that also advised them to reduce their saturated fat intake to less than 10% of total calories.

  • The group receiving personalized diet advice did a better job of reducing both saturated and total fat intake and maintaining that change for 12 months compared to the group that just received a set diet plan.
  • These results suggest that personalization of diet advice may improve long-term adherence to healthy dietary changes.

The authors of the study concluded: “Weight management interventions guided by nutrigenomics can motivate long-term improvements in dietary fat intake above and beyond gold-standard population-based interventions.”

There are, however, several caveats to this conclusion.

  • Participants in this study received both nutritional and psychological support throughout the 12-month program. We don’t know how well participants would have stuck with the program if they had not been continually reminded that the program had been personalized for them.
  • Participants in this study were well-educated, highly motivated, Caucasian women. We don’t know whether these results apply to men and to other ethnic and socioeconomic groups.
  • This study only looked at personalized diet advice based on DNA testing. Some studies suggest that other methods of diet personalization may also improve adherence.
  • Personalization can be misused to recommend unhealthy dietary changes. It is not enough to follow personalized diet advice. You also need to ask whether it is healthy dietary advice.

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.

Can You Improve Your Healthspan?

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Can You Live Healthier, Longer?

Ever since Ponce de Leon led an expedition to the Florida coast in 1513, we have been searching for the mythical “Fountain Of Youth”. What does that myth mean?

Supposedly, just by immersing yourself in that fountain you would be made younger. You would experience all the exuberance and health you enjoyed when you were young. There have been many snake oil remedies over the years that have promised that. They were all frauds.

But what if you had it in your power to live longer and to retain your youthful health for most of those extra years. The ability to live healthier longer is something that scientists call “healthspan”. But you can think of it as your personal “Fountain Of Youth”.

Where are we as a nation? Americans ranked 53rd in the world for life expectancy. We have the life expectancy of a third-world country. We are in sore need of a “Fountain Of Youth”.

That is why I decided to share two recent studies from the prestigious Harvard T.H. Chan School of Public Health with you today.

How Were The Studies Done?

Clinical StudyThese studies started by combining the data from two major clinical trials:

  • The Nurse’s Health Study, which ran from 1980 to 2014.
  • The Health Professional’s Follow-Up Study, which ran from 1986-2014.

These two clinical trials enrolled 78,865 women and 42,354 men and followed them for an average of 34 years. During this time there were 42,167 deaths. All the participants were free of heart disease, type 2 diabetes, and cancer at the time they were enrolled. Furthermore, the design of these clinical trials was extraordinary.

  • A detailed food frequency questionnaire was administered every 2-4 years. This allowed the investigators to calculate cumulative averages of all dietary variables.
  • Participants also filled out questionnaires that captured information on disease diagnosis every 2 years with follow-up rates >90%. This allowed the investigators to measure the onset of disease for each participant during the study. More importantly, 34 years is long enough to measure the onset of diseases like heart disease, diabetes, and cancer – diseases that require decades to develop.
  • The questionnaires also captured information on medicines taken and lifestyle characteristics such as body weight, exercise, smoking and alcohol use.
  • For analysis of diet quality, the investigators use something called the “Alternative Healthy Eating Index”. [The original Healthy Eating Index was developed about 10 years ago based on the 2010 “Dietary Guidelines for Americans”. Those guidelines have since been updated, and the “Alternative Healthy Eating Index” is based on the updated guidelines.] You can calculate your own Alternative Healthy Eating Index below, so you can see what is involved.
  • Finally, the investigators included five lifestyle-related factors – diet, smoking, physical activity, alcohol consumption, and BMI (a measure of obesity) – in their estimation of a healthy lifestyle. Based on the best available evidence, they defined “low-risk” in each of these categories. Study participants were assigned 1 point for each low-risk category they achieved. Simply put, if they were low risk in all 5 categories, they received a score of 5. If they were low risk in none of the categories, they received a score of 0.
  • Low risk for each of these categories was defined as follows:
    • Low risk for a healthy diet was defined as those who scored in the top 40% in the Alternative Healthy Eating Index.
    • Low risk for smoking was defined as never smoking.
    • Low risk for physical activity was defined as 30 minutes/day of moderate or vigorous activities.
    • Low risk for alcohol was defined as 0.5-1 drinks/day for women and 0.5-2 drinks/day for men.
    • Low risk for weight was defined as a BMI in the healthy range (18.5-24.9 kg/m2).

Can You Live Healthier Longer?

Older Couple Running Along BeachThe investigators compared participants who scored as low risk in all 5 categories with participants who scored as low risk in 0 categories (which would be typical for many Americans). For the purpose of simplicity, I will refer to people who scored as low risk in 5 categories as having a “healthy lifestyle” and those who scored as low risk in 0 categories as having an “unhealthy lifestyle”.

The results of the first study were:

  • Women who had had a healthy lifestyle lived 14 years longer than women with an unhealthy lifestyle (estimated life expectancy of 93 versus 79).
  • Men who had a healthy lifestyle lived 12 years longer than men with an unhealthy lifestyle (estimated life expectancy was 87 versus 75).
  • It was not necessary to achieve a perfect lifestyle. Life expectancy increased in a linear fashion for each low-risk lifestyle behavior achieved.

The authors of the study concluded: “Adopting a healthy lifestyle could substantially reduce premature mortality and prolong life expectancy in US adults. Our findings suggest that the gap in life expectancy between the US and other developed countries could be narrowed by improving lifestyle factors.”

The results of the second study were:

  • Women who had a healthy lifestyle lived 11 years longer free of diabetes, heart disease, and cancer than women who had an unhealthy lifestyle (estimated disease-free life expectancy of 85 years versus 74 years).
  • Men who had a healthy lifestyle lived 8 years longer free of diabetes, heart disease, and cancer than men who had an unhealthy lifestyle (estimated disease-free life expectancy of 81 years versus 73 years).
  • Again, disease-free life expectancy increased in a linear fashion for each low-risk lifestyle behavior achieved.

The authors concluded: “Adherence to a healthy lifestyle at mid-life [They started their analysis at age 50] is associated with a longer life expectancy free of major chronic diseases. Our findings suggest that promotion of a healthy lifestyle would help reduce healthcare burdens through lowering the risk of developing multiple chronic diseases, including cancer, cardiovascular disease, and diabetes, and extending disease-free life expectancy.”

Can You Improve Your Healthspan?

Questioning ManI posed the question at the beginning of this article, “Can you improve your healthspan?” These two studies showed that you can improve both your life expectancy and your disease-free life expectancy. So, the answer to the original question appears to be, “Yes, you can improve your healthspan. You can create your personal “Fountain of Youth.”

However, as a nation we appear to be moving in the wrong direction. The percentage of US adults adhering to a healthy lifestyle has decreased from 15% in 1988-1992 to 8% in 2001-2006.

The clinical trials that these studies drew their data from were very well designed, so these are strong studies. However, like all scientific studies, they have some weaknesses, namely:

  • They looked at the association of a healthy lifestyle with life expectancy and disease-free life expectancy. Like all association studies, they cannot prove cause and effect.
  • The clinical trials they drew their data with included mostly Caucasian health professionals. The results may differ with different ethnic groups.
  • These studies did not look at the effect of a healthy lifestyle on the onset of Alzheimer’s disease and other forms of dementia. However, other studies have shown that people who were low risk for each of the 5 lifestyle factors (diet, exercise, body weight, smoking, and alcohol use) individually have a reduced risk of developing Alzheimer’s and/or dementia.

Finally, I know you have some questions, and I have answers.

Question: What about supplementation? Will it also improve my healthspan?

Answer: When the investigators analyzed the data, they found that those with the healthiest lifestyles were also more likely to be taking a multivitamin. So, they attempted to statistically eliminate any effect of supplement use on the outcomes. That means these studies cannot answer that question.

However, if you calculate your Alternate Healthy Eating Index below, you will see that most of us fall short of perfection. Supplementation can fill in the gaps.

Question: I cannot imagine myself reaching perfection in all 5 lifestyle categories? Should I even try to achieve low risk in one or two categories?

Answer: The good news is that there was a linear increase in both life expectancy and disease-free life expectancy as people went from low-risk in one category to low-risk in all 5 categories. I would encourage you to try and achieve low risk status in as many categories as possible, but very few of us, including me, achieve perfection in all 5 categories.

Question: I am past 50 already. Is it too late for me to improve my healthspan?

Answer: Diet and some of the other lifestyle behaviors were remarkably constant over 34 years in both the Nurse’s Health Study and the Health Professional’s Follow-Up Study. That means that the lifespan and healthspan benefits reported in these studies probably resulted from adhering to a healthy lifestyle for most of their adult years.

However, it is never too late to start improving your lifestyle. You may not achieve the full benefits described in these studies, but you still can add years and disease-free years to your life.

How To Calculate Your Alternative Healthy Eating Index

You can calculate your own Alternative Healthy Eating Index score by simply adding up the points you score for each food category below.

Vegetables

Count 2 points for each serving you eat per day (up to 5 servings).

One serving = 1 cup green leafy vegetables or ½ cup for all other vegetables.

Do not count white potatoes or processed vegetables like French fries or kale chips.

Fruits

Count 2½ points for each serving you eat per day (up to 4 servings).

One serving = 1 piece of fruit or ½ cup of berries.

          (do not count fruit juice or fruit incorporated into desserts or pastries). 

Whole Grains

Count 2 points for each serving you eat per day (up to 5 servings).

One serving = ½ cup whole-grain rice, bulgur and other whole grains, cereal, and pasta or 1 slice of bread.

(For processed foods like pasta and bread, the label must say 100% whole grain).

Sugary Drinks and Fruit Juice

Count 10 points if you drink 0 servings per week.

Count 5 points for 3-4 servings per week (½ serving per day).

Count 0 points for 7 or more servings per week (≥1 serving per day).

One serving = 8 oz. fruit juice, sugary soda, sweetened tea, coffee drink, energy drink, or sports drink.

Nuts, Seeds and Beans

Count 10 points if you eat 7 or more servings per week (≥1 serving per day).

Count 5 points for 3-4 servings per week (½ serving per day).

Count 0 points for 0 servings per week.

One serving = 1 oz. nuts or seeds, 1 Tbs. peanut butter, ½ cup beans, 3½ oz. tofu.

Red and Processed Meat

Count 10 points if you eat 0 servings per week.

Count 7 points for 3-4 servings per week (½ serving per day).

Count 3 points for 3 servings per week (1 serving per day).

Count 0 points for ≥1½ servings per day.

One serving = 1½ oz. processed meats (bacon, ham, sausage, hot dogs, deli meat)

          Or 4 oz. red meat (steak, hamburger, pork chops, lamb chops, etc.)

Seafood

Count 10 points if you eat 2 servings per week.

Count 5 points for 1 serving per week.

Count 0 points for 0 servings per week.

1 serving = 4 oz.

Now that you have your total, the scoring system is:

  • 41 or higher is excellent
  • 37-40 is good
  • 33-36 is average (remember that it is average to be sick in this country)
  • 28-32 is below average
  • Below 28 is poor

Finally, for the purposes of these two studies, a score of 37 or higher was considered low risk.

The Bottom Line

Two recent studies have developed a healthy lifestyle score based on diet, exercise, body weight, smoking, and alcohol use. When they compared the effect of lifestyle on both lifespan (life expectancy) and healthspan (disease-free life expectancy), they reported:

  • Women who had had a healthy lifestyle lived 14 years longer than women with an unhealthy lifestyle.
  • Men who had a healthy lifestyle lived 12 years longer than men with an unhealthy lifestyle.
  • Women who had a healthy lifestyle lived 11 years longer free of diabetes, heart disease, and cancer than women had an unhealthy lifestyle.
  • Men who had a healthy lifestyle lived 8 years longer free of diabetes, heart disease, and cancer than men who had an unhealthy lifestyle.
  • It is not necessary to achieve a perfect lifestyle. Lifespan and healthspan increased in a linear fashion for each low-risk lifestyle behavior (diet, exercise, body weight, smoking, and alcohol use) achieved.
  • These studies did not evaluate whether supplement use also affects healthspan.
    • However, if you calculate your diet with the Alternate Healthy Eating Index they use (see above), you will see that most of us fall short of perfection. Supplementation can fill in the gaps.

The authors concluded: “Our findings suggest that promotion of a healthy lifestyle would help reduce healthcare burdens through lowering the risk of developing multiple chronic diseases, including cancer, cardiovascular disease, and diabetes, and extending disease-free life expectancy.”

For more details, including how to calculate whether you are low risk in each of the 5 lifestyle categories, 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?

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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.

Which Foods Should I Avoid?

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What Is Nutritionism?

In Defense Of FoodRecently, I have been reading Michael Pollan’s book “In Defense of Food”. Yes, I know the book has been around for a long time. Normally I read the scientific literature rather than popular health books. However, in the past few weeks I have had a lot more time to read books, so I decided to read this one.

Some of the things he says are “off the wall”. As he readily admits, he isn’t a scientist or a medical doctor. However, a lot of what he says is “right on”. He echoes many of the things I have been talking about for years. But he does a masterful job of pulling everything together into a framework he calls “nutritionism”.

If you have a chance, I highly recommend that you read his book.

I will briefly summarize his discussion of nutritionism below. I will also share some scientific support for what he is saying. Finally, I will close by sharing what the Bible says on the subject.

What Is Nutritionism?

Low Fat LabelSimply put, nutritionism is the belief that we can understand food solely in terms of its nutritional and chemical constituents and our requirements for them. I use the term “belief” purposely. As Michael Pollan puts it: “As the ‘-ism’ suggests, nutritionism is not a scientific subject, but an ideology.”

What Michael Pollan is referring to is taking food constituents like saturated fats, cholesterol, sugar, carbohydrates, polyunsaturated fats, monounsaturated fats, fiber, antioxidants, and probiotics and labeling them as either “good” or “bad”.

As he points out, that leads to debacles like the creation of margarine as a substitute for butter. Of course, everyone reading this article knows that we subsequently found out that the trans fat in margarine was worse for us than the saturated fat in butter. He offers many other examples like this.

He also points out that the nutritionism concept has given free rein to the food industry to replace whole foods with processed foods that are cholesterol-free, sugar-free, low-fat, low-carb, or high in fiber, omega-3s, etc. He says that these foods are seldom healthier than the foods they replace. I agree.

Finally, he points out that the scientific support for the classification of individual ingredients or foods as “good” or “bad” is weak. That’s because when scientists design a study that removes a chemical constituent or a food from the diet, they have to replace it with something. And what they replace it with determines the outcome of the study. I give some examples of this in the next section.

The essence of Michael Pollan’s message is:

  • The effect of an individual nutrient or chemical constituent on your health depends on the food it is found in. Forget the fancy nutrition labels. Whole foods are almost always healthier than processed foods.
  • The effect of a food or food constituent on your health also depends on your overall diet. We should be thinking about healthy diets rather than the latest “magical” or “forbidden” food.

I will discuss these points below.

Which Foods Should I Avoid?

Question MarkNow, let’s get to the question, “Which Foods Should I Avoid?” If we are talking about whole foods, the short answer is “None”. As I said in my book, “Slaying The Food Myths”, “We have 5 food groups for a reason”.

For example, if we are talking about plant foods, each plant food group:

  • Has a unique blend of vitamins and minerals.
  • Has a unique blend of phytonutrients.
  • Has a unique blend of fiber.
  • Supports the growth of a unique combination of beneficial gut bacteria.
  • Dr Strangelove and his friends are telling you to eliminate whole grains, fruits, and legumes (beans) from your diet. Recent studies suggest that might not be a good idea. Here is one example.

If we are talking about animal foods, each animal food group:

  • Has a unique blend of vitamins and minerals.
  • May have unique components that are important for our health. [Note: This is an active area of research. Theories have been proposed for which components in animal foods may be important for our health, but they have not been confirmed.]
  • Vegan purists will tell you that you have no need for meat and dairy foods. Recent studies suggest otherwise. Here is one example.

With that as background, let’s turn our attention to nutritionism and look at some of science behind claims that certain food components are either good for us or bad for us.

Saturated Fat. Saturated fat is the poster child for nutritionism.lowfat

First, we were told by the American Heart Association and other health organizations that saturated fat was bad for us. Recently Dr. Strangelove and his friends are telling us that saturated fat is good for us. Instead of limiting saturated fat, we should be limiting carbs by cutting out fruits, whole grains, and legumes. Both cite clinical studies to support their claims. How can this be?

Perhaps a little history is in order. When the American Heart Association recommended that we decrease intake of saturated fat, they were envisioning that we would replace it with monounsaturated and polyunsaturated fat in the context of a healthy diet of fruits, vegetables, whole grains, and legumes. That never happened.

Big Food quickly realized that if the American public were to follow the AHA guidelines, it would be disastrous for their bottom line. So, they sprang into action. They mixed sugar, white flour, and a witch’s brew of chemicals to create highly processed, low fat “foods”. Then they told the American public, “Don’t worry. You don’t have to give up your favorite foods. We have created low fat alternatives.”

This is the essence of what Michael Pollan refers to as nutritionism. By marketing their fake foods as low fat Big Food created the halo of health. In fact, Big Food’s fake foods were less healthy than the foods they replaced. Americans got fatter and sicker.

Now let’s look at the conflicting claims that saturated fat is bad for us or good for us. How can clinical studies disagree on such an important question? The answer is simple. It depends on what you replace it with. You need to consider saturated fat intake in the context of the overall diet.

I discussed this in a previous issue of “Health Tips From the Professor”, but let me summarize it briefly here. The American Heart Association tells us that replacing half of the saturated fat in a typical American diet with:

  • Trans fats, increases heart disease risk by 5%.
  • Refined carbohydrates and sugars (the kind of carbohydrates in the typical American Diet), slightly increases heart disease risk.
  • Complex carbohydrates (whole grains, fruits & vegetables), decreases heart disease risk by 9%.
  • Monounsaturated fats (olive oil & peanut oil), decreases heart disease risk by 15%.
  • Polyunsaturated fats (vegetable oils and fish oil), decreases heart disease risk by 25%.
  • Unsaturated fats in the context of a Mediterranean diet, decreases heart disease risk by 45%.

My advice: Saturated fat is neither good for you nor bad for you. A little bit of saturated fat in the context of a healthy diet is fine. A lot of saturated fat in the context of an unhealthy diet is problematic.

fatty steakRed Meat. Is red meat bad for you? Like saturated fat, it depends on the amount of red meat and the overall diet. I covered this in detail in “Slaying The Food Myths”, but let me summarize briefly here:

According to the World Health Organization, red meat is a probable carcinogen. If we look at the postulated mechanisms by which it causes cancer, they can be mostly neutralized by components of various plant foods.

My advice: An 8-ounce steak with fries and a soda is probably bad for you. Three ounces of that same steak in a green salad or stir fry may be good for you.

I should make one other point while I am on the topic. Dr. Strangelove and his friends have been telling you that grass-fed beef is better for you than conventionally raised beef. Once again, that is nutritionism.  Grass-fed beef is lower in saturated fat and high in omega-3s than conventionally raised beef. That may be better for your heart, but it has no effect on the cancer-causing potential of red meat. It doesn’t give the license to eat 8-ounce steaks on a regular basis. You still want to aim for 3-ounces of that grass-fed beef in a green salad or stir fry. 

High-Fructose Corn Syrup. This one seems to be on everyone’s “naughty list”. You are being told to read labels, and if the food has high-fructose corn syrup on the label, put it back on the shelf. But is that good advice?

It turns out that all the studies on the bad effects of high-fructose corn syrup have been done with sodas and highly processed foods. This should be your first clue.

Of course, as soon as high-fructose corn syrup gained its “bad” reputation, Big Food started replacing it with Sugar Comparisons“heathier” sugars. Does that make those foods healthier?

The answer is a clear “No”. Both chemically and biologically, high-fructose corn syrup is identical to sucrose (table sugar), honey, molasses, maple syrup, coconut sugar, date sugar, or grape juice concentrate. Agave sugar is even higher in fructose than high-fructose corn syrup. This is your second clue.

Substituting these sugars for high-fructose corn syrup doesn’t turn sodas and processed foods into health foods. This is nutritionism at its worst.

My advice: Forget reading the label. Forget trying to avoid foods with high-fructose corn syrup. Avoid sodas and processed foods instead.

Sugar. Once the public started to realize that natural sugars in processed foods were just as bad for us as high-fructose corn syrup, sugars became “bad”. We were told to avoid all foods containing sugar in any form. In fact, we were told we needed to become “label detectives” and recognize all the deceptive ways that sugar could be hidden on the label.

Apple With Nutrition LabelI have discussed this in detail in a previous issue of “Health Tips From The Professor”.

Let me just summarize that article with one quote, “It’s not the sugar. It’s the food. There is the same amount and same types of sugar in an 8-ounce soda and a medium apple. Sodas are bad for you, and apples are good for you.” If you are wondering why that is, I have covered it in another issue of “Health Tips From the Professor”.

Before leaving this subject, I should mention that nutritionism has risen its ugly head here as well. Big Food has struck again. They have replaced sugar with a variety of artificial sweeteners.

Once again, nutritionism has failed. Those artificially sweetened sodas and processed foods are no healthier and no more likely to help you keep the weight off than the sugar-sweetened foods they replace. I have covered the science behind that statement in several previous issues of “Health Tips From the Professor”. Here is one example.

My advice: Forget about sugar phobia. You don’t need to become a label detective. Just avoid sodas, sugar-sweetened beverages, and sweet processed foods. Get your sugar in its natural form in fruits and other whole foods.

low carb dietCarbs. Dr. Strangelove and his friends are now telling you that you need to avoid all carbs. That is pure nutritionism. Carbs are neither good nor bad. It depends on the type of carb and what you replace it with.

Once again, clinical studies have given conflicting outcomes. Each side of the carbohydrate debate can provide clinical studies to support their position. How can that be? The answer is simple. It depends on what assumptions went into the design of the clinical studies. I have written several articles on this topic in “Health Tips From the Professor”, but let me give you one example here.

In this example, I looked at two major studies. The PURE (Prospective Urban Rural Epidemiology) study included data from 135,000 participants in 18 countries. In this study, the death rate decreased as the % carbohydrate in the diet decreased. The low-carb enthusiasts were doing a victory dance.

However, it was followed by a second, even larger study. The ARIC (Atherosclerosis Risk In Communities) study included 432,000 participants from even more countries. In this study, the death rate decreased as the % carbohydrate decreased to about 40%. Then a curious thing happened. As the % carbohydrate in the diet decreased further, the death rate increased.

How can you explain this discrepancy? When you examine the PURE study:

  • The % carbohydrate only ranged from 70% to 40%.
  • The data for the PURE study was obtained primarily with third world countries. That is an important distinction because:
    • In those countries, it is primarily the well to do that can afford sodas, processed foods, and meat.
    • The poor subsist on what they can grow and inexpensive staples like beans and rice.
  • Simply put, in the PURE study, the type of carbohydrate changed as well as the amount of carbohydrate.
    • At the highest carbohydrate intakes, a significant percentage of the carbohydrate came from sugar and refined grains.
    • At the lowest carbohydrate intakes, most of the carbohydrate intake came from beans, whole grains, and whatever fruits and vegetables they could grow.

When you examine the ARIC study:how much carbohydrates should we eat aric

  • The % carbohydrate ranged from 70% to 20%.
  • The ARIC study added in data from the US and European countries. That is an important distinction because:
    • Low carb diets like Atkins and Keto are popular in these countries. And those are the diets that fall into the 20-40% carbohydrate range.
    • Most people can afford diets that contain a lot of meat in those countries.
  • Simply put, at the lower end of the scale in the ARIC study, people were eating diets rich in meats and saturated fats and eliminating healthy carbohydrate-containing foods like fruits, whole grains and legumes.

My advice: The lesson here is to avoid simplistic nutritionism thinking and focus on diets rather than on foods. When you do that it is clear that carbs aren’t bad for you, it’s unhealthy carbs that are bad for you.

Which Foods Should I Avoid? By now the answer to the question, “Which Foods Should I Avoid?” is clear. Avoid sodas, sugar-sweetened beverages and processed foods (The term processed foods includes convenience foods, junk foods, and most sweets).

What Does This Mean To You?

Questioning ManNow that we are clear on which foods you should avoid, let’s look at the flip side of the coin. Let’s ask, “Which foods should you include in your diet?

As I said at the beginning of this article, “We have 5 food groups for a reason”. We should consider whole foods from all 5 food groups as healthy.

Of course, each of us is different. We all have foods in some food groups that don’t treat us well. Some of us do better with saturated fats or carbs than others. We need to explore and find the foods and diets that work best for us.

However, whenever we assume one diet is best for everyone, we have crossed the line into nutritionism.

What Does The Bible Say?

Let me start this section by saying that I rely on the Bible for spiritual guidance rather than nutritional guidance. However, as part of our church’s Bible reading plan, I was reading 1 Timothy. A passage from 1 Timothy 4:1-5 leapt out at me. It reinforces the theme of Michael Pollan’s book and seems uniquely applicable to the times we live in.

“The Spirit clearly says that in later times some will abandon the faith and follow deceiving spirits and things taught by demons. Such teachings come through hypocritical liars, whose consciences have been seared as with a hot iron. They…order people to abstain from certain foods, which God created to be received with thanksgiving by those who believe and who know the truth. For everything God created is good, and nothing is to be rejected if it is received with thanksgiving, because it is consecrated by the word of God and prayer.”

Interesting.

The Bottom Line

In this article, I have discussed the concept of “nutritionism” introduced in Michael Pollan’s book “In Defense Of Food”. He defines nutritionism as the belief that we can understand food solely in terms of its nutritional and chemical constituents and our requirements for them.

What Michael Pollan is referring to is taking food constituents like saturated fats, cholesterol, sugar, carbohydrates, polyunsaturated fats, monounsaturated fats, fiber, antioxidants, and probiotics and labeling them as either “good” or “bad”. He points out that when we accept these simplistic labels, we often end up creating foods and diets that are less healthy than the ones we were trying to replace.

At the beginning of the article, I asked the question, “Which Foods Should I Avoid?” I then looked at several foods or food groups we have told to avoid, including saturated fats, red meat, high-fructose corn syrup, sugar, and carbs. When you look at the science behind these recommendations from the lens of nutritionism, you come to two conclusions:

  • We should avoid sodas, sugar-sweetened beverages and processed foods (The term processed foods includes convenience foods, junk foods, and most sweets).
  • Whole foods from all 5 food groups should be considered as healthy.

Of course, each of us is different. We all have foods in some food groups that don’t treat us well. Some of us do better with saturated fats or carbs than others. We need to explore and find the foods and diets that work best for us.

However, whenever we assume one diet is best for everyone, we have crossed the line into nutritionism.

For more details and a bible verse that supports the theme of Michael Pollan’s book and seems uniquely applicable to the times we live in, 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.

Health Tips From The Professor