Is Fructose Good For You Or Bad For You?

Is It The Fructose Or Is It The Food?

Author: Dr. Stephen Chaney

VillainFructose is the villain of the day. It is #1 on everyone’s “No-No” list. Almost every website, blog, and diet book demonize it. Even authors I highly respect say we should absolutely avoid it.

We are told it causes obesity, diabetes, heart disease, and non-alcoholic fatty liver disease – a disease that was unheard of only a few decades ago. We are told to read labels and avoid any foods with fructose or high-fructose corn syrup listed on their label.

But wait. Isn’t fructose a natural sugar? The answer is, “Yes”. It is the main sugar in fruit and many other naturally sweet whole foods. In fact, there is the same amount of fructose in an 8-ounce soda and a medium apple.

Does that mean that fruits are also bad for us? What is the truth?

Is It The Fructose Or Is It The Food?

AppleLet me put this into perspective for you. I have covered this in detail in a previous issue of Health Tips From The Professor. Here is a brief summary.

  • There are no sugar villains. There are no sugar heroes. Most of your favorite “natural” sugars are chemically and biologically indistinguishable from high-fructose corn syrup. Other natural sugars, like agave sugar, contain more fructose than high-fructose corn syrup.
  • All the studies showing the bad effects of fructose have been done with sodas and/or highly processed foods with added sugar. Let’s be clear. Those foods are bad for you.
  • Fruits, on the other hand, are good for you. You’ve heard the old adage, “An apple a day keeps the doctor away”. A recent study showed that isn’t just an “old wives’ tale”. It is true.

Why is that? Why is fructose in sodas and junk foods bad for us and fructose in fruits good for us?

Part of the answer is that fruits are high in fiber, which slows the release of fructose into the intestine as fruits are digested. In addition, the fructose in fruits is trapped in a cellular matrix, which also slows the release of fructose during digestion.

Sodas and highly processed foods, on the other hand, have nothing to slow the release of fructose. It is immediately available as soon as the food reaches the intestine.

A recent study sheds light on why the rate of fructose release in our intestine may be important. The study showed:

  • When fructose is released slowly our bodies know exactly what to do with it.
    • Most of it is metabolized by the cells that line our intestine, and the rest is metabolized by the liver.
    • In both cases fructose is converted to glucose and slowly released into the bloodstream.
    • This stabilizes blood sugar levels.
  • When fructose is released quickly our bodies are overwhelmed and bad things happen.
    • The intestine passes the excess on to the liver, and the liver converts it to fat rather than glucose.
    • The fat is stored in the liver.
    • This leads to insulin resistance, diabetes, heart disease, and fatty liver disease.

But could the fiber in fruits have other beneficial effects such as supporting populations of beneficial gut bacteria? The study ( J Beisner et al, Nutrients, 12: 3444, 2020) I will focus on today suggests the answer is yes.

How Was The Study Done?

Clinical StudyInvestigators from the University of Hohenheim, Germany recruited 12 healthy female volunteers, ages 20 – 40 (average age = 28).

Each of the subjects was given a series of diets to follow for one week each.

  • Week one was a low fructose diet (10 g of fructose/day). For this diet phase subjects had to avoid sweets, highly processed foods, sodas, and fruits and vegetables containing more than 1 g of fructose per serving.
  • Week two was a high fructose fruit diet (100 g of fructose/day). This diet phase emphasized fructose-rich fruits and vegetables. Sweets, highly processed foods, and sodas had to be avoided.
  • Week three was a repeat of the low fructose diet (10 g of fructose/day).
  • Week four was a high-fructose corn syrup diet (100 g of fructose/day). For this diet phase subjects had to sweeten the food they were eating with a measured amount of high-fructose corn syrup. They also had to avoid fructose-rich fruits and vegetables.

The diets were designed to have around 2,000 calories/day and to have the same amounts of fat (30% of calories), protein (15% of calories), and carbohydrate (55% of calories). However, the fiber content of the diets was very different (around 17 g/day on the low fructose and high-fructose corn syrup diets and around 38 g/day on the high fructose fruit diet).

The subjects were given detailed instructions and training before starting on the 4-week program. They also kept a daily dietary record of everything they ate and drank so the investigators would know how closely they stuck to their dietary instructions.

This experimental design was based on previous studies showing that populations of gut bacteria change within 24-48 hours when you go on a new diet. Stool samples were collected at the end of each week and analyzed for gut bacteria.

Is Fructose Good For You Or Bad For You?

MicrobiomeThe study showed:

  • Consumption of a high-fructose, fruit-rich diet resulted in:
    • An increase in beneficial butyrate-producing bacteria (more about that below).
    • A decrease in bacteria associated with elevated total and LDL cholesterol.
    • Decreased blood levels of total and LDL cholesterol.
  • Consumption of a high-fructose corn syrup diet had the opposite effect. It resulted in:
    • A decrease in beneficial butyrate-producing bacteria.
    • An increase in bacteria associated with elevated total and LDL cholesterol.
    • Increased blood levels of total and LDL cholesterol.

The authors concluded: “We provide evidence that the high-fructose corn syrup diet induces an imbalanced microbiota [gut bacteria] profile characterized by a significantly reduced abundance of beneficial butyrate-producing bacteria and of bacteria known for anti-obesity effects…Despite the high fructose content, the fruit-rich diet shifts the intestinal microbiota composition in a protective manner…”

The authors said that there were probably two mechanisms for the different effects of fructose in high-fructose corn syrup and in fruits.

  • The fiber found in fruit supports the growth of beneficial bacteria in our intestine.
  • When high-fructose corn syrup is present in foods with low fiber content, it is released rapidly in the intestine. As I noted above, the cells that line our intestine become overwhelmed and pass some of that excess fructose on to our liver. However, the authors cited previous studies showing that some of that excess fructose remains in our intestine and supports the growth of unhealthy bacteria.

What Does Butyrate Do?

Question MarkYou are probably wondering what is special about butyrate-producing bacteria. Here is a brief synopsis.

  • Butyrate is a short chain fatty acid. As you might expect from its name, it was originally identified as a constituent of butter.
  • Some species of gut bacteria convert the fats in our diet to butyrate.
    • It is used as a preferred energy source for the cells that line our intestine. Consequently, butyrate production in our intestines has been linked to:
      • Reduced inflammation of the cells lining our intestine, which reduces the risk for diseases like inflammatory bowel disease (IBS) and Crohn’s Disease.
      • Reduced risk of “leaky gut syndrome”.
      • Reduced risk of colon cancer.
    • It is also absorbed into the bloodstream and appears to affect several metabolic pathways. For example, butyrate production in the intestine is associated with:
      • Decreased cholesterol levels.
      • Improved blood sugar control.
      • A healthy body weight.

What Does This Mean For You?

Questioning ManThis was a small study. As the authors noted, larger studies of longer duration are needed to confirm that the effects of fructose on our gut bacteria depend on the food the fructose is in. However, several other studies have come to similar conclusions.

More importantly, this study merely shows that the effect of fructose-containing foods on our gut bacteria is a potential mechanism for explaining why the effect of fructose depends on the food it is in.

There is already overwhelming evidence that fructose in fruits is good for us, while high-fructose corn syrup in sodas and highly processed foods is bad for us.

Does that mean high-fructose corn syrup is villainous? Should we read labels and avoid any food containing high-fructose corn syrup?

I would remind you that the amount of fructose and the relative abundance of fructose and glucose are virtually identical in fruits and high-fructose corn syrup. It is not high-fructose corn syrup that is the problem, it is the foods it is found in.

We don’t need to become compulsive label readers. We just need to eat more foods without labels.

The Bottom Line 

High-fructose corn syrup has been vilified in recent years. However, there is increasing evidence that it is not fructose that is the problem. It is the foods it is found in.

A recent study was designed to test that hypothesis. The investigators fed subjects high fructose diets in which the fructose came either from fruits or high-fructose corn syrup. The amount of fructose was identical in the two diets. The investigators then asked what effect the two diets had on gut bacteria. In short:

  • Consumption of the high-fruit diet increased healthy levels of beneficial gut bacteria and suppressed levels of unhealthy gut bacteria.
  • Consumption of the high-fructose corn syrup diet had the opposite effect. It increased unhealthy bacteria and suppressed beneficial bacteria.

The authors concluded: “We provide evidence that the high-fructose corn syrup diet induces an imbalanced microbiota [gut bacteria] profile characterized by a significantly reduced abundance of beneficial…bacteria and of bacteria known for anti-obesity effects…Despite the high fructose content, the fruit-rich diet shifts the intestinal microbiota composition in a protective manner…”

My take is as follows: This study shows that the effect of fructose-containing foods on our gut bacteria is a potential mechanism for explaining why the effect of fructose depends on the food it is in.

There is already overwhelming evidence that fructose in fruits is good for us, and high-fructose corn syrup in sodas and highly processed foods is bad for us.

Does that mean that high-fructose corn syrup is villainous? Should we read labels and avoid any food containing high-fructose corn syrup?

I would remind you that the amount of fructose and the relative abundance of fructose and glucose is virtually identical in fruits and high-fructose corn syrup. It is not high-fructose corn syrup that is the problem, it is the foods it is found in.

We don’t need to become compulsive label readers. We just need to eat more foods without labels.

For more details read the article above.

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

Does Vitamin D Prevent Type 1 Diabetes?

Does Genetics Influence Supplementation Benefits?

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

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

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

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

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

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

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

In this article, I will answer 3 questions:

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

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

Does Genetics Influence Supplementation Benefits?

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

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

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

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

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

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

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

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

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

Biochemistry 101: Vitamin D Metabolism

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

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

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

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

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

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

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

How Was This Study Done?

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

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

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

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

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

This study was remarkable for two reasons:

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

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

Does Vitamin D Prevent Type 1 Diabetes?

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

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

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

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

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

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

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

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

What Does This Study Mean For You?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The Bottom Line

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

This study found that:

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

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

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

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

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

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

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

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

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

Why Do Diet Sodas Make You Fat?

Is Mixing Diet Sodas With Carbs Bad For You?

Why Do Sodas Cause Obesity?Many people, and many doctors, believe that diet sodas and artificially sweetened foods are a healthy choice. After all:

  • Cutting calories by drinking diet sodas and eating artificially sweetened foods should help you lose weight.
  • If sugar is the problem for diabetics, diet sodas and artificially sweetened foods should be a healthier choice.

On the surface, these ideas appear to be self-evident. They seem to be “no-brainers”. The truth, however, is more complicated.

When studies are tightly controlled by dietitians so that the people consuming diet sodas don’t add any extra calories to their diet, the results are exactly as expected. People consuming diet sodas lose weight compared to people drinking regular sodas.

However, as I have described in an earlier issue of “Health Tips From the Professor”, the results are different in the real world where you don’t have a dietitian looking over your shoulder. In those studies, diet sodas are just as likely to cause weight gain as regular sodas.

As Barry Popkin, a colleague at the University of North Carolina, put it” “The problem is that we [Americans] are using diet sodas to wash down our Big Macs and fries.” In short, people drinking diet sodas tend to increase their caloric intake by adding other foods to their diet. Even worse, the added foods aren’t usually fruits and vegetables. They are highly processed junk foods.

Why is that? The short answer is that nobody knows (more about that later). However, a recent study (JR Dalenberg et al, Cell Metabolism, 31: 493-502, 2020) suggests an unexpected mechanism for the weight gain associated with diet soda consumption. Let’s look at that study.

How Was The Study Done?

Clinical StudyThe study recruited 45 healthy young adults (ages 20-45) who habitually consumed less than 3 diet sodas a month. They were randomly assigned to three groups. The participants in each group came into the testing facility seven times over a span of 2 weeks. Each time they were given 12 ounces of one of three equally sweet tasting beverages in a randomized, double-blind fashion.

  • Group 1 received a sucralose-sweetened drink contained 0.06 grams of sucralose (equivalent to two packets of Splenda).
  • Group 2 received a sugar-sweetened drink contained 7 teaspoons of sucrose (table sugar).
  • Group 3 received a combo drink contained 0.06 grams of sucralose plus 7 teaspoons of maltodextrin. Maltodextrin is a water-soluble carbohydrate that does not have a sweet taste.

o   Maltodextrin was used because Splenda and most other commercial sucralose products contain it along with sucralose. You need something to fill up those little sucralose-containing packets.

o   This drink was included as a control. The expectation was that it would give the same results as the sucralose-sweetened drink.

Three measurements were performed prior to and following the 2-week testing period:

  • An oral glucose tolerance test in which participants drink a beverage containing a fixed amount of glucose. Then their blood sugar and blood insulin levels are measured over the next two hours.

o   This is a measure of how well they were able to control their blood sugar levels.

  • A test in which they were given samples that had either a sweet, sour, salty, or savory taste. Then:

o   They were asked to identify each taste and report how strong the taste was.

o   MRI scans of their brains were performed to determine how strongly their brains responded to each of the tastes.

Is Mixing Diet Soda With Carbs Bad For You?

The results were surprising. The first surprise came when the investigators unblinded the results of the oral glucose tolerance test:

  • Blood sugar and blood insulin responses were unaffected by the 2-week exposure to sugar-sweetened drinks.

o   This was expected.

  • Blood sugar and blood insulin were relatively unaffected by the 2-week exposure to sucralose-sweetened drinks. If anything, the control of blood sugar levels was slightly improved at the end of two weeks.

o   This was a disappointment for the investigators. One of the prevailing theories is that artificially sweetened beverages alter the blood sugar response. The investigators found no evidence for that idea.

  • Following the 2-week exposure to the combo drinks (sucralose plus maltodextrin), blood sugar levels were unaffected, but blood insulin levels were increased. This implies that more insulin was required to control blood sugar levels. In other words, these participants had developed insulin resistance.

o   This result was unexpected. Remember the investigators had included this drink as a control.

o   The investigators pointed out that the insulin resistance associated with the sucralose-maltodextrin combo could increase the risk of type 2 diabetes and obesity.

  • Because of this unexpected result, the investigators did a follow-up study in which participants were given a maltodextrin-only drink using the same study protocol. The oral glucose tolerance test was unchanged by the 2-week exposure to maltodextrin-only drinks.

When the investigators conducted taste tests, the ability of participants to taste all four flavors was unchanged by a 2-week exposure to any of the drinks.

However, when the investigators did MRI scans to measure the brain’s response to these flavors:

  • A two-week exposure to the sucralose plus maltodextrin drinks reduced the brain’s response to sweet but not to any of the other flavors.

o   In other words, the subjects could still taste sweet flavors, but their brains were not responding to the sweet taste. Since sweetness activates pleasure centers in the brain this could lead to an increased appetite for sweet-tasting foods.

o   This might explain the weight gain that has been observed in many previous studies of diet sodas.

  • Two-week exposures to the other drinks had no effect on the brain’s response to any of the flavors. Once again, this effect was only seen in the sucralose-maltodextrin combination.

The investigators concluded:

  • “Consumption of sucralose combined with carbohydrates impairs insulin sensitivity…and…neural responses to sugar.
  • Insulin sensitivity is not altered by sucralose or carbohydrate consumption alone.
  • The results suggest that consumption of sucralose in the presence of a carbohydrate dysregulates gut-brain regulation of glucose metabolism.”

The investigators pointed out that this could have several adverse consequences. Again, in the words of the authors:

“Similar exposure combinations (artificial sweeteners plus carbohydrates) almost certainly occur in free-living humans, especially if one considers the consumption of a diet drink along with a meal. This raises the possibility that the combination effect may be a major contributor to the rise in incidence of type 2 diabetes and obesity. If so, addition of artificial sweeteners to increase the sweetness of carbohydrate-containing food and beverages should be discouraged and consumption of diet drinks with meals should be counseled against.”

Why Do Diet Sodas Make You Fat?

As I mentioned at the start of this article, there are a lot of hypotheses as to why diet sodas make us fat. These hypotheses break down into two classifications: psychological and physiological.

The psychological hypothesis is easiest to explain. Essentially, it goes like this: We feel virtuous for choosing a zero-calorie sweetener, so we allow ourselves to eat more of our favorite foods. It is unlikely that this hypothesis holds for all diet soda drinkers. However, it is also hard to exclude it as at least part of the explanation for the food overconsumption associated with diet soda use.

There are multiple physiological hypotheses. Most of them are complicated, but here are simplified explanations of the three most popular hypotheses:

  • The sweet taste of artificial sweeteners tricks the brain into triggering insulin release by the pancreas. This causes blood sugar levels to plummet, which increases appetite.
  • The sweet taste of artificial sweeteners is not appropriately recognized by the brain. This diminishes release of hormones that suppress appetite.
  • Artificial sweeteners interfere with insulin signaling pathways, which leads to insulin resistance.

There is some evidence for and against each of these hypotheses.

However, this study introduces a new physiological hypothesis – namely that it is the combination of artificial sweeteners and carbohydrates that results in a dysregulation of the normal mechanisms controlling appetite and blood sugar.

What Does This Study Mean For You?

Diet Soda DangersLet’s start with the obvious. This is just a hypothesis.

  • This was a very small study. Until it is confirmed by other, larger studies, we don’t know whether it is true.
  • This study only tested sucralose. We don’t know whether this applies to other artificial sweeteners.
  • The study only tested maltodextrin in combination with sucralose. We don’t know whether it applies to other carbohydrates.

Therefore, in discussing how this study applies to you, let’s consider two possibilities – if it is true, and if it is false.

If this hypothesis is true, it is concerning because:

  • We often consume diet sodas with meals. If, for example, we take the earlier example of a diet soda with a Big Mac and fries, both the hamburger bun and the fries are high carbohydrate foods.

 

  • Sucralose and other artificial sweeteners are used in low calorie versions of many carbohydrate rich processed foods.

If this hypothesis is false, it does not change the underlying association of diet soda consumption with weight gain and type 2 diabetes. It is merely an attempt to explain that association. We should still try to eliminate diet sodas and reduce our consumption of artificially sweetened, low calorie foods.

My recommendation is to substitute water and other unsweetened beverages for the diet drinks or sugar sweetened beverages you are currently consuming. If you crave the fizz of sodas, drink carbonated water. If you need more taste, try herbal teas or infuse water with slices of lemon, lime, or your favorite fruit. If you buy commercial brands of flavored water, check the labels carefully. They may contain sugars or artificial sweeteners. Those you want to avoid.

The Bottom Line

Many studies have called into question the assumption that diet sodas and diet foods help us lose weight. In fact, most of these studies show that diet soda consumption is associated with weight gain rather than weight loss.

There are many hypotheses to explain this association, but none of them have been proven at present.

This study introduces a new hypothesis – namely that the combination of artificial sweeteners and carbohydrates results in a dysregulation of the normal mechanisms controlling appetite and blood sugar. In particular, this study suggested that combining sucralose with carbohydrates caused insulin resistance and reduce the ability of the brain to respond appropriately to sweet tastes.

The authors concluded: “Similar exposure combinations (artificial sweeteners plus carbohydrates) almost certainly occur in free-living humans, especially if one considers the consumption of a diet drink along with a meal. This raises the possibility that the combination effect may be a major contributor to the rise in incidence of type 2 diabetes and obesity. If so, addition of artificial sweeteners to increase the sweetness of carbohydrate-containing food and beverages should be discouraged and consumption of diet drinks with meals should be counseled against.”

If this hypothesis is true, it is concerning because:

  • We often consume diet sodas with meals. If, for example, we take the example of a diet soda with a Big Mac and fries, both the hamburger bun and the fries are high carbohydrate foods.
  • Artificial sweeteners are used in low calorie versions of many carbohydrate rich processed foods.

If this hypothesis is false, it does not change the underlying association of diet soda consumption with weight gain and type 2 diabetes. It is merely an attempt to explain that association. We should still try to eliminate diet sodas and reduce our consumption of artificially sweetened, low calorie foods.

My recommendation is to substitute water and other unsweetened beverages for the diet drinks or sugar sweetened beverages you are currently consuming. If you crave the fizz of sodas, drink carbonated water. If you need more taste, try herbal teas or infuse water with slices of lemon, lime, or your favorite fruit. If you buy commercial brands of flavored water, check the labels carefully. They may contain sugars or artificial sweeteners. Those you want to avoid.

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.

Do Artificial Sweeteners Help You Lose Weight?

Sucralose and Weight Loss

Author: Dr. Stephen Chaney

 

Do artificial sweeteners help you lose weight?

It’s a puzzle. We are drinking more artificially sweetened foods and sodas than ever. We’ve been told that those artificially sweeteners will help us cut calories and keep us slender. Yet, surprisingly, we’re fatter than ever.

Let me put some numbers to that statement. The number of people consuming calorie free sodas in the US alone increased from 70 million to 260 million between 1987 and 2000. During that same time period, the percentage of overweight adults in this country increased from 52% to 66%; the percentage of obese adults increased from 20% to 32%; and the percentage of obese children increased from 10% to 17%. Clearly something isn’t working.

And, it may just be the artificial sweeteners that aren’t working. A study published in 2007 (R. Dingra et al, Circulation, 116: 480-484, 2007 ) showed that people consuming regular (sugar containing) sodas were 48% more likely to become obese over a four-year period than people who primarily drank water. That wasn’t surprising. The surprising finding from this study was that people who consumed diet sodas were just as likely to become obese as those drinking regular sodas.

Now you may be saying: “Wait a minute. I thought I read that consuming diet sodas actually helps people lose weight.” The answer is that in those studies dietitians rigorously controlled the caloric intake from other foods so that the only caloric difference was between the diet sodas and the regular sodas. Under those conditions the results are fairly obvious. Fewer calories from sodas = weight loss. But those aren’t the results that you see in free living populations where you don’t have a dietitian peering over your shoulder. In those populations people consuming diet sodas tend to take in the same number of total calories overall and gain just as much weight as people drinking regular sodas.

 

Do Artificial Sweeteners Prevent Weight Loss?

 

Obviously, people consuming diet sodas which contain artificial sweeteners must compensate by consuming extra calories from other foods. But, why are they consuming those extra calories? Some experts hypothesize that the answer is physiological. The sweet taste of the diet sodas triggers the release of insulin, which drives down blood sugar levels and makes people hungrier. Other experts hypothesize that the answer is psychological. People simply feel virtuous for consuming the diet sodas and feel they can now splurge somewhere else.

do artificial sweeteners help you lose weightAnimal studies have suggested that the cause may actually be physiological. Those studies have shown that there are “sweetness receptors” in the intestine that respond to the sweetness of sugars and trigger an increase in the level of proteins that transport sugars from the intestine into the bloodstream. That makes great sense from an evolutionary point of view. If we’re eating a low carbohydrate diet we really don’t want to waste a lot of energy producing proteins that transport sugars into our bloodstream. However, whenever we eat foods high in carbohydrates we don’t want to waste that carbohydrate. So, our intestine rapidly breaks the carbohydrates down to simple sugars, and our body responds by increasing our ability to transport those simple sugars into the bloodstream.

This can lead to blood sugar swings and increased food cravings. You’ve heard about the blood sugar swings associated with meals high in simple sugars. When sugars enter the bloodstream very rapidly, blood sugar levels increase, which causes insulin to be secreted. The insulin drives down blood sugar levels, leading to hypoglycemia and increased hunger. That’s a highly simplified scenario, but you get the general idea.

Now the interesting thing is that animal studies have suggested that artificial sweeteners are also recognized by the intestinal “sweetness receptors”. So artificial sweeteners also trigger an increase in the intestinal sugar transporters and prime the body so that blood sugar swings are more likely to occur whenever we eat carbohydrates.

While the results from animal studies have been very consistent with this model, the results from human clinical studies have been mixed. Some studies have suggested that artificial sweeteners do increase the likelihood of blood sugar swings, while other studies have reported that artificial sweeteners have no effect on blood glucose and insulin levels.

With this in mind, do artificial sweeteners help you lose weight?  Let’s continue to investigate.

 

Do Artificial Sweeteners Help You Lose Weight?

 

A recent study (M.Y. Pepinoet al, Diabetes Care, 36: 2530-2535, 2013 ) provides a possible explanation for these conflicting results. This study was similar to many of the previous studies in that obese adults were given either sucralose (an artificial sweetener) or water 10 min before being given a fixed amount of glucose, and blood sugar and insulin levels were followed over the next five hours. What made this study unique was that overweight participants were selected who did not normally consume artificially sweetened beverages or foods (Those people are hard to find in the overweight US population).

artificial sweetenersAnd the results were fairly clear-cut. The participants consuming sucralose prior to the glucose load had a 20% greater increase in blood sugar levels, a 20% greater increase in the amount of insulin produced, and significantly lower blood sugar levels three hours after the glucose load than participants consuming water prior to the glucose load. In the words of the authors: “These data suggest that sucralose ingestion is not physiologically inert but affects the glycemic [blood sugar] response to oral glucose load and potentiates glucose stimulated insulin secretion in obese people.” Basically, what they are saying is that sucralose primes their bodies so that they are more likely to experience blood sugar swings when they subsequently consume carbohydrates. [And that can lead to food cravings and weight gain.]

The authors hypothesized that some previous studies had not found an effect of artificial sweeteners on blood sugar and insulin levels because most of the people in those studies were already consuming artificially sweetened beverages on a regular basis and their intestinal sugar transport proteins were already maximally stimulated. Basically, what they are saying is that when someone is regularly consuming artificial sweeteners the damage has already been done (sugar transport is already maximal), and a single dose of an artificial sweetener will not have any significant additional effect.

So, do artificial sweeteners help you lose weight?  I think you know.

 

The Bottom Line

 

It has become clear in recent years that artificially-sweetened diet sodas and diet foods are not effective at preventing weight gain, and may, in fact, contribute to weight gain. There is also increasing evidence that artificially-sweetened diet sodas may be harmful to our health. In fact, an international consortium of obesity experts recently concluded: “The absence of evidence to support the role of artificially sweetened beverages in preventing weight gain and the lack of studies on their long-term effects on health strengthen the position that artificially-sweetened beverages should not be promoted as part of a healthy diet.”

 

However, the reason why diet sodas appear to promote obesity rather than prevent it has remained elusive.

  • A recent study suggests that sucralose (and presumably other artificial sweeteners) triggers a complex serious of metabolic responses that lead to increased appetite and food cravings.
  • However, this is just one small study. Many more studies will be required before we understand why artificial sweeteners promote obesity, rather than prevent it.
  • However, it is clear that artificial sweeteners are not the simple, magical solutions for weight control that food manufacturers and advertisers would have you believe.
    • There are unresolved safety issues with all the artificial sweeteners – but that’s another subject for another day.
    • There is no convincing evidence that artificial sweeteners actually help you lose weight unless you are very carefully controlling the calories from all the other foods you’re eating – and if you’re doing that successfully, you probably don’t need artificial sweeteners in the first place.
    • There is some evidence that artificial sweeteners may actually cause blood sugar swings and make you hungrier, thus making it harder – not easier – to control your weight.
  • The best solution to weight control is always true lifestyle change that includes exercise, healthy foods, and reduced caloric intake and is not based on gimmicks or artificial ingredients.

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.

Which Foods Lower Blood Sugar?

Can You Believe The “Experts”?

Author: Dr. Stephen Chaney

which foods lower blood sugarYour blood sugar levels have been creeping up. Your doctor has been bugging you to do something about it – even threatening to put you on medications if you don’t get your blood sugar under control. So, which foods lower blood sugar?

Now it’s the first of the year, and you’ve vowed to do something about it. You have vowed to make better food choices. That should be easy. There is lots of great advice about foods that lower blood sugar on the internet. For example, in a recent search, I found articles proclaiming “9 foods that lower blood sugar”, “7 foods that control blood sugar”, and “12 power foods to beat diabetes”.

But, are those foods the right ones for you? What if we are remarkably different in our blood sugar responses to the same food? This is just what a recent study suggests.

How Was The Study Designed?

A group of scientists in Isreal set out to test the hypothesis that people eating identical meals might have a high variability in their post-meal blood glucose response (Zeevi et al, Cell, 163, 1079-1094, 2015).

measure glucoseThe investigators enrolled 800 subjects ages 18-70 into their study. None of the individuals had diabetes. However, 54% of them were overweight (BMI ≥ 25 kg/m2) and 22% of them were obese (BMI ≥ 30 kg/m2). Thus, their subject population was typical of the adult population of almost every Western, industrialized country.

All 800 subjects were followed for one week during which time:

  • They were connected to a continuous glucose monitor, which measured their blood glucose levels every 5 seconds.
  • They were given a Smartphone app and instructed to log their food intake, exercise, and sleep in real time.
  • They were told to follow their normal daily routine and dietary habits except for the first meal of every day, which consisted of five different types of standardized “meals” (glucose, fructose, bread, bread with butter, bread with chocolate), all providing 50 gm of available carbohydrate.

The glucose monitor recorded blood sugar responses for 2 hours following each meal. From that information, the investigators calculated a PPGR (post-prandial glycemic response), which I will mercifully refer to as “blood sugar response”, for every meal eaten by every subject throughout the week.

The standardized “meals” eaten at the beginning of the day were used to validate the study. For example:

  • Two of the standardized meals were given to each subject twice during the study separated by at least one day.
    • There was very little variability in blood sugar response when the same standardized meal was given to the same subject on different days.
    • However, there was a significant amount of variability in blood sugar response when the same standardized meal was given to different subjects.
  • The average blood sugar response to each of the standardized meals was very similar to literature values from previous studies (Most previous studies have reported only average blood sugar responses, not individual variability).

In short, the results from the standardized “meals” validated both the reliability and reproducibility of the data.

Finally, to eliminate as many confounding variables as possible, the investigators compared blood sugar response only for those meals in which a single food was the major component of the meal and that food provided 20-40 gm of carbohydrate.

Here is where things got really interesting!

Which Foods Lower Blood Sugar?

breadThis study showed that there is tremendous individual variability in the blood sugar response to any given food. For example, individual blood sugar responses varied by:

  • 4-fold for sugar-sweetened soft drinks, grapes and apples.
  • 5-fold for rice.
  • 6-fold for bread and potatoes.
  • 7-fold for ice cream and dates.

Put another way:

  • Some people had almost no blood sugar response to cookies, but a very high blood sugar response to a banana.
  • Other people had almost no blood sugar response to bananas, but a very high blood sugar response to cookies.

That is a pretty striking result. Which foods lower blood sugar? This study suggests that some people trying to control their blood sugar can eat bananas, while others should avoid them. It might even mean that some people trying to control blood sugar can eat cookies. I know that is what many people would like to hear, but I’m not ready to make that recommendation.

Why Is There So Much Individuality in Blood Sugar Response?

good food choicesYou are probably wondering why there is such variability in blood sugar response to the same foods. There are several factors that influence individual blood sugar response. For example,

  • Overweight and obesity (Both tend to increase blood sugar response).
  • Dietary habits (Meats, particularly fatty meats, processed grains, and simple sugars tend to increase blood sugar response to a given amount of carbohydrate. Unprocessed grains, fresh fruits & vegetables tend to decrease blood sugar response to a given amount of carbohydrate).
  • What we eat with a given meal (Protein, fiber, and fat in a meal can decrease blood sugar response to the carbohydrate in that meal).
  • Physical activity (Increased muscle mass decreases blood sugar response to a given amount of carbohydrate).
  • The bacteria in our intestine (This may be a chicken-and egg thing. The bacteria in our intestine are influenced by our dietary habits.)
  • Genetics.
  • Things we don’t yet know about.

The good news is that we can actually control some of these variables. The ones over which we have the most control are weight, dietary habits, what we eat along with the carbohydrates in our meals, and physical activity.

What Does This Mean For You?

blood sugarThe authors concluded that “universal dietary recommendations [for lowering blood sugar levels] may have limited utility.”  That is because dietary recommendations are based on average responses and none of us are average. As the saying goes “We are all wonderfully [and differently] made”.

So, when you read about diets and foods that will help you keep your blood sugar levels under control, take those recommendations with a grain of…sugar. They are a good starting place, but you need to listen to your body, and eat the foods that work best for you.  So, which foods lower blood sugar?  It is different for different people, but there are some variables you can control.

Don’t get carried away, however. I’m pretty sure Twinkies washed down with a soft drink are bad for just about everyone.

More importantly, control the variables you can – weight, dietary habits, foods you eat along with carbohydrates, and physical activity. If you control those four variables, you will be well on your way to ideal blood sugar control.

 

The Bottom Line

 

  • A recent study has shown that there is tremendous variability in blood sugar response to identical meals from one individual to the next.
  • The authors of the study concluded that “universal dietary recommendations [for lowering blood sugar levels] may have limited utility.” That is because dietary recommendations are based on average responses, and none of us are average.
  • So, when you read about diets and foods that will help you keep your blood sugar levels under control, take those recommendations with a grain of…sugar. They are a good starting place, but you need to listen to your body, and eat the foods that work best for you.
  • There are variables influencing our blood sugar response that we cannot control, such as genetics. However, there are some very important variables that we can control. For example, we can improve our blood sugar response by:
    • Attaining and maintaining ideal weight. Losing as little as 5-10 pounds can result in a significant improvement.

 

    • Eating a diet that emphasizes fresh fruits & vegetables, nuts, and whole grains and minimizes meats, especially fatty meats, processed grains, and simple sugars. This may act by influencing the bacteria that populate our intestine.

 

    • Consuming carbohydrates along with protein, fiber-rich foods, and even some fat in the same meal.

 

    • Increasing physical activity, especially activity that increases lean muscle mass.

 

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