Do Processed Foods Increase Your Risk Of Diabetes?

Why Do We Keep Eating Processed Foods?

Fast Food DangersUnless you are Rip Van Winkle and have been asleep for the past 20 years you probably know that the highly processed foods in the typical American diet are bad for your health. But perhaps you didn’t realize just how bad they were.

But first, let’s start with a bit of perspective. Scientists like to be precise. Even healthy foods go through some processing.

  • The oatmeal you ate this morning was either steel-cut or ground. That is processing.
  • The almond butter you put on your whole grain toast this morning was made by roasting and grinding. That is processing.

So, scientists have developed the term “ultra-processed food” to describe the worst of the worse. In short, ultra-processed foods:

  • Usually go through several physical and chemical processes, such as extruding, molding, prefrying, and hydrogenation that can lead to the formation of toxic contaminants. One example you may have heard about recently would be acrylamide in French fries.
  • Typically contain ingredients of no or little nutritive value, such as refined sugar, hydrogenated oils, emulsifiers, artificial sweeteners, thickening agents, and artificial colors. Some of these ingredients have been linked to cancer, heart disease, and premature death.
  • Have long shelf-lives because of added preservatives. This allows migration of chemicals such as bisphenol A from the packaging materials into the food.

Examples of ultra-processed foods include:

  • Sodas
  • Chips
  • Candy and packages of cookies or crackers
  • Most breakfast cereals
  • Boxed cake, cookie, and pancake mix
  • Chicken nuggets and fish sticks
  • Fast food burgers
  • Hot dogs and other processed meats
  • Infant formula
  • Instant noodles
  • Most store-bought ice cream
  • Flavored yogurt

In short, ultra-processed foods include sodas and the junk and convenience foods Americans hold so dear. Even things like infant formula and flavored yogurt make the list.

Evidence of the ill effects of ultra-processed foods on our health is becoming overwhelming. In previous issues of “Health Tips From the Professor” I have shared recent studies that have shown that heavy consumption of ultra-processed foods is linked to increased risk of obesity and cancer. Other studies have linked ultra-processed food consumption with increased risk of depression, heart disease, and premature death.

In this issue of “Health Tips From the Professor” I:

  • Ask the important question, “If we know these foods are so bad for us, why do we still keep eating them?”

How Was The Study Done?

Clinical StudyThe data from this study were taken from an ongoing study in France (the NutriNet-Sante study) looking at associations between nutrition and health. This study began enrolling French adults 18 and older in 2009.

This is a web-based study. Participants are prompted to go to a dedicated website and fill out questionnaires related to things like sex, age, height, weight, smoking status, physical activity, health status, and diet.

With respect to diet, participants filled out a series of 3 nonconsecutive 24-hour dietary records at the time of enrollment and every 6 months. This is a particularly strong feature of this study. Many studies of this type only analyze participant’s diets at the beginning of the study. Those studies have no way of knowing how the participant’s diets may have changed during the study.

Diagnosis of type 2 diabetes for study participants was obtained from the French centralized health records.

The study enrolled 104,708 participants, 20% men and 80% women, and followed them for an average of 6 years. The average age of the participants was 43 years.

Do Processed Foods Increase Your Risk Of Diabetes?

High Blood SugarIn this study the range of ultra-processed foods in the French diet ranged from 7% to 27% (average = 17%). High intake of ultra-processed foods was associated with:

  • Younger participants. Simply put, young people were more likely to drink sodas and eat junk food than older adults.
  • Increased caloric intake. Ultra-processed foods have a higher caloric density than whole, unprocessed foods.
  • No surprise here. Previous studies have shown that ultra-processed food consumption increases the risk of obesity.
  • Poorer diet quality. Again, no surprise. Junk foods tend to crowd healthier foods out of the dirt. Specifically, ultra-processed food consumption was associated with:
    • Higher intake of sugar and salt.
    • Lower intake of fiber.
    • Higher intake of sugary drinks, red and processed meats.
    • Lower intake of whole grains, yogurt, nuts, fruits, and vegetables.

However, even after statistically correcting for all these factors, there was a significant association between ultra-processed food consumption and the onset of type 2 diabetes in the 6-year follow-up period.

  • There was a linear relation between ultra-processed food consumption and the development of type 2 diabetes. Simply put, the more ultra-processed food the participants consumed the more likely they were to be diagnosed with type 2 diabetes.
  • There was a 15% increased risk of developing type 2 diabetes for every 10% increase in ultra-processed food consumption.

The authors concluded:

“In this large observational prospective study, a higher proportion of ultra-processed food in the diet was associated with a higher risk of type 2 diabetes. Even though these results need to be confirmed in other populations and settings, they provide evidence to support efforts by public health authorities to recommend limiting ultra-processed food consumption.”

What Does This Study Mean For You?

Questioning WomanYou might be tempted to say that a 15% increase in the risk of developing diabetes is a small price to pay for continuing to eat the foods you enjoy. However, you should be alarmed by this study. Here is why.

The French diet is much healthier than the American. Remember that ultra-processed foods only comprised 17% of the French Diet. In contrast, a recent survey found that:

  • Ultra-processed foods make up 58% of the average American’s diet.
  • Ultra-processed foods account for 90% of the added sugar in our diet.

It is no wonder that obesity and diabetes are reaching epidemic proportions in our country.

You might also be tempted to think that you can just take some medications and live with type 2 diabetes. However, you should think of type 2 diabetes as a gateway disease. It increases your risk of heart disease, high blood pressure, Alzheimer’s disease, kidney damage, and neuropathy, just to name a few. These are diseases that make your life miserable and ultimately kill you.

More importantly, type 2 diabetes is completely reversible if you catch it early enough. Just lose some weight, exercise more, give up the ultra-processed foods, and eat a healthy diet. I recommend a whole food, primarily plant-based diet.

Why Do We Keep Eating Processed Foods?

Fast FoodsWe all know that ultra-processed foods are bad for us. Study after study show that they make us sick. They kill us prematurely. And, unlike most topics in the field of nutrition, this is not controversial.

For example, there have been lots of bizarre diets that have come and gone over the years. There have been books written on “The Steak Lover’s Diet” and “The Drinking Man’s Diet”. But nobody has written a book on “The Junk Food Lover’s Diet”. It simply would not be believable.

So why do we Americans keep eating such unhealthy foods. Part of the answer is physiological. A preference for sweet, salty, and fatty foods is hardwired into our brain. That’s because they had great survival value in prehistoric times.

If we think back to the time when we were hunters and gatherers:

  • Fruits are healthy foods. They are a great source of antioxidants, phytonutrients, and fiber, but there were no orchards or grocery stores back then. We had to search for fruits in the wild. Our desire for sweet tasting foods provided the motivation to seek them out.
  • Game was seasonal and sometimes scarce. We had to be prepared to go for days or weeks without eating except for the leaves and roots we could gather. Our bodies are designed to store fat as the primary energy source to get us through the lean times. Our preference for fatty foods encouraged us to store as much fat as possible in times of plenty so we would be prepared for times of scarcity.
  • If we fast forward to our early recorded history, salt was scarce. It was worth its weight in gold. Yet some salt is essential for life. Our preference for salty foods encouraged us to search out supplies of salt.

Unfortunately, the food industry has weaponized these food preferences to create the ultra-processed foods we know today. Their ads entice us by associating these foods with youth and good times. And ultra-processed foods have become ubiquitous. There are fast food restaurants on almost every street corner and shopping mall in the country.

Fortunately, we do not have to let the food industry destroy our health. We can retrain our taste buds to appreciate the sweetness of fresh fruits and vegetables. We can substitute healthy fats for the kinds of fat found in most ultra-processed foods. We can also retrain our taste buds to appreciate herbs and spices with just a pinch of salt.

The Bottom Line

Ultra-processed foods, such as sodas, junk foods, and convenience foods have become the biggest food group in the American diet. A recent study found:

  • Ultra-processed foods make up 58% of the average American’s diet.
  • Ultra-processed foods account for 90% of the added sugar in our diet.

That is scary because ultra-processed foods are deadly. Previous studies have shown that consumption of ultra-processed foods is linked to obesity, heart disease, cancer, and Alzheimer’s disease.

The study discussed this week looked at the association between ultra-processed food consumption and type 2 diabetes. It showed:

  • There was a linear relation between ultra-processed food consumption and the development of type 2 diabetes. Simply put, the more ultra-processed food the participants consumed the more likely they were to be diagnosed with type 2 diabetes.
  • There was a 15% increased risk of developing type 2 diabetes for every 10% increase in ultra-processed food consumption.

You might be tempted to think that you can just take some medications and live with type 2 diabetes. However, you should think of type 2 diabetes as a gateway disease. It increases your risk of heart disease, high blood pressure, Alzheimer’s disease, kidney damage, and neuropathy, just to name a few. This are diseases that make your life miserable and ultimately kill you.

More importantly, type 2 diabetes is completely reversible if you catch it early enough. Just lose some weight, exercise more, give up the ultra-processed foods, and eat a healthy diet. I recommend a whole food, primarily plant-based diet.

For more details and a discussion of why Americans continue to eat ultra-processed food even though we know it is bad for us, 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.

How Much DHA Is Needed To Prevent Alzheimer’s

What Are We Missing?

Cognitive-DeclineWe are an aging population. As such, issues like cognitive decline, dementia, and Alzheimer’s Disease are of increasing concern. After all, what is the good of reaching your “Golden Years” with a healthy body if you lose your mind?

The ability of the omega-3 fatty acids DHA and EPA to reduce the risk of cognitive decline, dementia, and Alzheimer’s Disease is controversial. Some studies say yes. Others say no.

When studies are conflicting most experts simply conclude the treatment is unproven. I am sympathetic to that viewpoint, but I first like to ask the questions: “Why are the studies conflicting? What are we missing?”

I start by evaluating the strengths and weaknesses of the individual studies.

  • If the studies claiming the treatment works are weak, I am content to “join the chorus” and consider the treatment unproven.
  • If the studies claiming the treatment doesn’t work are weak, I am a strong advocate for more well-designed studies before we conclude that the treatment doesn’t work.
  • If both the “pro” and “con” studies are strong, I want to ask, “What are we missing?”

This is the situation with studies asking whether DHA reduces the risk of Alzheimer’s Disease and other forms of cognitive decline as we age.

  • Association studies show that greater intake and higher blood levels of the omega-3 fatty acids EPA and DHA are associated with lower risk of Alzheimer’s Disease.
  • However, most placebo-controlled clinical trials with either DHA alone or DHA + EPA have come up negative. Of course, one can always argue that most of the placebo-controlled clinical trials were too short or too small to show a statistically significant effect. But, my question remains, “What else are we missing?”

One recent study has provided an interesting clue. The authors of the study postulated that B vitamins were required to deliver omega-3 fatty acids to the brain, and their study showed that omega-3 fatty acids were only effective at decreasing the risk of cognitive decline in subjects who also had optimal B vitamin status.

In other words, this study suggested that studies on the effect of omega-3 supplementation and risk of developing Alzheimer’s are doomed to failure if a significant percentage of the subjects have sub-optimal B vitamin status.

The authors of the current study ( IC Arellanes et al, EBioMedicine, doi.org/10.1016/j.ebiom.2020.102883) proposed two additional hypotheses for the negative results of previous clinical trials and designed an experiment to test their hypotheses. Their hypotheses were:

  • Uptake of DHA and EPA by the brain is very inefficient, and previous studies have not used sufficient doses of DHA or DHA plus EPA to see a significant effect on cognitive impairment.
  • The APOE4 gene further decreases the uptake of DHA and EPA by the brain.

Before I describe how the study was done, I should probably provide some context by describing how DHA and EPA reach the brain and the role of the apoE protein in the process. It’s time for my favorite topic: “Biochemistry 101”.

Biochemistry 101: What Does The ApoE Protein Do?

ProfessorIf you have ever tried to mix oil and water, it should come as no surprise to you that fats, including DHA and EPA, and cholesterol are not water soluble. That leaves our bodies with a dilemma. How do they get the fat and cholesterol we eat to pass through our bloodstream and get to our cells, where they are needed?

Our body’s solution is to incorporate the fat and cholesterol into particles called lipoproteins. Lipoprotein particles sequester the fat and cholesterol in their interior and surround them with water soluble phospholipids and proteins. Lipoproteins allow our bodies to transport fat and cholesterol through our bloodstream to the tissues that need them.

The next question, of course, is how the lipoproteins know which cells need the fat and cholesterol. This is where apoproteins like apoE come into play. We can think of the apoE protein as a zip code that directs lipoproteins to cells with an apoE receptor.

Our nervous system contains lots of apoE receptors, and binding of the apoE protein to its receptor is instrumental in the delivery of DHA, EPA, and cholesterol to our nervous system.

DHA and cholesterol are both important for brain health. That is because they are major components of the myelin sheath that wraps around our neurons and protects them. EPA may also be important for brain health because its anti-inflammatory effects are thought to prevent the accumulation of the amyloid plaques that are the hallmark of late-onset Alzheimer’s Disease.

There are three major versions of the APOE gene, APOE2, APOE3, and APOE4. Each of them plays slightly different roles in our body. However, it is the APOE4 version that is of interest to us. About 25% of us have the APOE4 version of the APOE gene and it increases our risk of developing Alzheimer’s Disease by a factor of two.

We do not know why this is, but one hypothesis is that lipoproteins with the apoE4 protein have more difficultly delivering much needed DHA, EPA, and cholesterol to the brain. This is one of the hypotheses that the authors set out to study.

How Was The Study Done?

Clinical StudyThere are two things you should know about this study.

  • This was a pilot study designed to test the author’s hypotheses and allow them to choose the correct dose of DHA to use for a subsequent study designed to test whether high-dose DHA can reduce the risk of developing Alzheimer’s Disease.
  • This was a very small study. That’s because the only way to determine how much DHA and EPA reaches the nervous tissue is to perform a lumbar puncture and obtain cerebrospinal fluid at baseline and again at the end of the study. Lumbar punctures are both painful and a bit risky. They were lucky to find 26 individuals who consented to the lumbar punctures.

This was a double-blind, placebo controlled clinical study.

  • Half the subjects were given 2,152 mg/day of DHA for 6 months, and half were given a daily placebo consisting of corn and soybean oil for 6 months.
  • Because previous studies have suggested that B vitamins were important for DHA and EPA uptake by nervous tissue, all subjects received a B vitamin supplement.
  • Levels of DHA and EPA were measured in both plasma and cerebrospinal fluid at baseline and again at the end of 6 months. Note: The subjects were only supplemented with DHA. The investigators were relying on the body’s ability to convert DHA into EPA.
  • All subjects were screened for APOE4

Other important characteristics of the study subjects were:

  • Average age was 69. They were 80% female.
  • All of them had a close family member who had previously been diagnosed with dementia, but none of them had been diagnosed with cognitive impairment at the time of entry into the study.
  • Around 45% of them had the APOE4 version of the APOE.

In other words, none of them currently had dementia, but most were at high risk of developing dementia.

How Much DHA Is Needed To Prevent Alzheimer’s?

fish and fish oilAfter 6 months of supplementing with over 2,000 mg/day of DHA:

  • DHA levels in the blood had increased by 200%.
  • However, DHA levels in cerebrospinal fluid had increased by only 28%.
  • Moreover, DHA levels in cerebrospinal fluid were 40% lower in subjects who had the APOE4 gene compared to subjects with the APOE2 and APOE3

EPA levels in cerebrospinal fluid averaged about 15-fold lower than DHA levels. When they looked at the effect of DHA supplementation on EPA levels.

  • EPA levels in plasma had increased by 50%.
  • EPA levels in cerebrospinal fluid had increased by 43%.
  • EPA levels in cerebrospinal fluid were 3-fold lower in subjects who had the APOE4 gene compared to subjects with the APOE2 and APOE3

The authors concluded:

“We observed only a modest (28%) increase in cerebrospinal fluid DHA levels with 2152 mg per day of DHA supplementation. This finding has implications for past clinical trials that have used lower doses (e.g. 1 g daily of DHA supplements or less) and were overwhelmingly negative. Using lower doses of omega-3 supplements may have resulted in limited omega-3 brain delivery.”

“Another aspect affecting the response to DHA supplementation is APOE4 status. Subjects with the APOE4 gene showed lower DHA levels and significantly lower EPA levels than subjects with other APOE genes”.

“In summary, our study suggests that higher doses of omega-3 fatty acids (2 or more g of DHA) are needed to ensure adequate brain delivery, particularly in APOE4 carriers…Past low dose (1 g per day or less) omega-3 supplementation trials in dementia prevention may not have provided adequate brain levels to fully evaluate the efficacy of omega-3 supplementation on cognitive outcomes.”

Based on the results from this study the authors are currently testing the effect of B vitamins and high dose DHA supplementation on cerebrospinal fluid fatty acid levels, brain imaging, and cognitive outcomes in a larger ongoing clinical trial.

What Does This Study Mean For You?

Questioning ManThe ability of the omega-3 fatty acids DHA and EPA to reduce the risk of cognitive decline, dementia, and Alzheimer’s Disease is confusing. Studies disagree.

In situations like this, most experts dismiss the hypothesis as “unproven”. However, I like to ask, “What are we missing?”

One recent study provided a clue. It suggested that omega-3s and B vitamins were interdependent. We need both to reduce cognitive decline. However, that might not be the complete answer.

This study gave both DHA and B vitamins to subjects and discovered another interesting clue. The study suggests we may not have been giving subjects enough omega-3s to see a significant effect on cognitive decline.

Let me start by saying this study did not test whether or not DHA supplementation prevents cognitive decline, dementia, and Alzheimer’s Disease. Nor does it tell us how much DHA is needed to prevent Alzheimer’s Disease, other than to show that anything less than 2 g per day is likely to be inadequate. 

However, the study did make two important advances:

#1: It showed just how difficult it is to deliver adequate amounts of DHA and EPA to the brain. This is important because it shows:

  • Most previous studies have not used high enough doses of DHA or DHA plus EPA to evaluate the effect of omega-3 fatty acids on cognitive decline. Those studies were not simply negative. They were doomed to failure. The studies were worthless.
  • That means we should stop saying that the ability of omega-3s to prevent cognitive decline and diseases like Alzheimer’s is unproven. Instead, we should say that hypothesis has not adequately been tested.
  • That also means future studies of the ability of DHA to reduce the risk of cognitive decline, dementia, and/or Alzheimer’s will need to use much higher doses or a better delivery system to get adequate amounts of DHA and EPA into the brain.

#2: It showed that the APOE4 gene significantly decreases the ability of the brain to accumulate DHA and EPA. This has several important implications.

  • Because both DHA and EPA are vital for brain health, this may explain why the APOE4 gene increases the risk of Alzheimer’s Disease.
  • It also means those at highest risk for Alzheimer’s Disease are the ones who are most likely to have difficulties accumulating DHA and EPA in their brain.
  • Once again, it means future studies of the ability of supplemental DHA to reduce the risk of Alzheimer’s Disease will need to use much higher doses of DHA.

The Bottom Line

We are an aging population. As such, issues like cognitive decline, dementia, and Alzheimer’s Disease are of increasing concern. After all, what is the good of reaching your “Golden Years” with a healthy body if you lose your mind?

The ability of the omega-3 fatty acids DHA and EPA to reduce the risk of cognitive decline, dementia, and Alzheimer’s Disease is controversial.

  • Association studies show that greater intake and higher blood levels of the omega-3 fatty acids EPA and DHA are associated with lower risk of Alzheimer’s Disease.
  • However, most placebo-controlled clinical trials with either DHA alone or DHA + EPA have come up negative.

In situations like this, most experts dismiss the hypothesis as “unproven”. However, I like to ask, “What are we missing?”

One recent study provided a clue. It suggested that omega-3s and B vitamins were interdependent. We need optimal amounts of both to reduce dementia. However, that might not be the complete answer.

This study gave both DHA and B vitamins to participants and discovered another interesting clue. The study suggests we may not have been giving subjects enough omega-3s to see a significant effect on cognitive decline.

The authors of the study hypothesized:

  • Uptake of DHA and EPA by the brain is very inefficient, and previous studies have not used sufficient doses of DHA or DHA plus EPA to see a significant effect on cognitive impairment.
  • The APOE4 gene, which is known to increase the risk of Alzheimer’s Disease, further decreases the uptake of DHA and EPA by the brain.

Their study confirmed their hypotheses and made two important advancements:

#1: It showed just how difficult it is to deliver adequate amounts of DHA and EPA to the brain. This is important because it shows:

  • Most previous studies have not used high enough doses of DHA or DHA plus EPA to evaluate the effect of omega-3 fatty acids on cognitive decline. Those studies were not simply negative. They were doomed to failure. The studies were worthless.
  • That means we should stop saying that the ability of omega-3s to prevent cognitive decline and diseases like Alzheimer’s is unproven. Instead, we should say that hypothesis has not adequately been tested.
  • That also means future studies of the ability of DHA to reduce the risk of cognitive decline, dementia, and/or Alzheimer’s will need to use much higher doses or a better delivery system to get adequate amounts of DHA and EPA into the brain.

#2: It showed that the APOE4 gene significantly decreases the ability of the brain to accumulate DHA and EPA. This has several important implications.

  • Because both DHA and EPA are vital for brain health, this may explain why the APOE4 gene increases the risk of Alzheimer’s Disease.
  • It also means those at highest risk for Alzheimer’s Disease are the ones who are most likely to have difficulties accumulating DHA and EPA in their brain.
  • Once again, it means future studies of the ability of supplemental DHA to reduce the risk of Alzheimer’s Disease will need to use much higher doses of DHA.

Based on the results from this study the authors are currently testing the effect of B vitamins and high dose DHA supplementation on DHA and EPA levels in the brain, brain imaging, and cognitive outcomes in a larger ongoing clinical trial.

For more details, read the article above. For a better understanding of the roles of DHA, EPA, and the APOE gene in brain health, you may want to read my “Biochemistry 101” section 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?

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.

Will A Healthy Lifestyle Help Prevent Alzheimer’s Disease?

Can Lifestyle Overcome Genetics?

Author: Dr. Stephen Chaney

 

Will a healthy diet help prevent Alzheimer’s disease?

world health organization alzheimersAlzheimer’s disease and other forms of dementia are among the most feared diseases of aging. What use is it to have a healthy body, a loving family, and a successful career if you can’t remember any of it? You should be able to enjoy your Golden years, not see them slip through your fingers.

If you have a family history of dementia or have sent your DNA off for testing and learned you are genetically predisposed to dementia, you are probably worried. You are not alone.

According to the World Health Organization:

  • 50 million people worldwide have dementia.
  • Alzheimer’s Disease accounts for 60-70% of all dementia cases.

According to the Alzheimer’s Association:

  • 8 million Americans are currently living with Alzheimer’s Disease.
  • 1 in 3 seniors will die from Alzheimer’s or another form of dementia.
  • The number of Americans with Alzheimer’s Disease is expected to increase to 14 million by 2050.

Perhaps the scariest thing about Alzheimer’s is that the medical community has no answers. There are no drugs to prevent or cure Alzheimer’s and brain transplants are out of the question. Some medical professionals will tell you nothing can be done, but is that true?

Studies have suggested that a healthy lifestyle can help reduce your risk of developing Alzheimer’s and other forms of dementia. But what about genetics? Will a healthy lifestyle only reduce your risk of dementia if your genetic risk is low or will it be equally effective when your genetic risk is high? Can lifestyle overcome genetics?

This study (I Lourida et al, JAMA, 322: 430-437, 2019 ) was designed to answer that important question.

How Was The Study Done?

alzheimers studyThis study used data collected from the UK Biobank study, which was designed to assess the effect of genetics and lifestyle on health outcomes. The UK Biobank study enrolled more than 500,000 participants between 2006 and 2010.

At the time of enrollment, UK Biobank participants were given a physical exam. Blood samples were taken and preserved for subsequent genetic analysis. They also completed an online questionnaire and were interviewed about lifestyle, medical history, and nutritional habits.

This study used a subset of the UK Biobank data, consisting of 196,383 people who were 60 years or older and free of cognitive impairment or dementia at the time of enrollment. They were followed for an average of 8 years.

The authors created the following scoring system to assess the effect of genetics and lifestyle on Alzheimer’s disease and dementia:

The Genetic Risk Score represents the combined effect of all genetic variants known to increase the risk of Alzheimer’s disease and dementia. [Note: There is no single gene that determines whether you will develop Alzheimer’s and other forms of dementia. There are multiple gene variations that affect your risk.]

The Healthy Lifestyle Score was based on 4 well-established dementia risk factors (smoking status, physical activity, diet, and alcohol consumption). The risk factors were defined as follows:

  • Smoking status was categorized as current or no current smoking.
  • Regular physical activity was defined as meeting the American Heart Association of:
  • ≥ 150 minutes of moderate exercise per week – OR –
  • ≥ 75 minutes of vigorous activity per week.

A healthy diet was defined as meeting at least 4 of these 7 criteria.

  • ≥ 3 servings/day of fruit.
  • ≥ 3 servings/day of vegetables.
  • ≥ 2 servings/week of fish.
  • ≥ 3 servings/day of whole grains.
  • ≤ 1 serving/week of processed meats.
  • ≤ 1.5 servings/week of red meat.
  • ≤ 1.5 servings/day of refined grains.

Moderate alcohol consumption was defined as:

  • Up to one drink a day for women.
  • Up to two drinks a day for men.

Finally, the diagnosis of Alzheimer’s Disease or dementia was obtained from the centralized databank of the UK National Health Service.

 

Will A Healthy Lifestyle Help Prevent Alzheimer’s Disease?

 

healthy-lifestyle-prevent-alzheimersHere are the results from the study:

  • People at high genetic risk were almost twice as likely to develop dementia as those at low genetic risk.

In other words, genetics matter. If you have “bad” genes, your risk of developing dementia is increased significantly.

  • A healthy lifestyle decreased the risk of developing dementia by about 40% for both people at high genetic risk and for people at low genetic risk.

In other words, lifestyle also matters. You can significantly decrease your risk of developing dementia, no matter what your genetic risk.

  • People at high genetic risk and an unhealthy lifestyle were almost three times more likely to develop dementia than people at low genetic risk and a healthy lifestyle.

In other words, the combination of a high genetic risk and an unhealthy lifestyle is the worst of all possible worlds.

  • People at low genetic risk and an unhealthy lifestyle were just as likely to develop dementia as people at high genetic risk and a healthy lifestyle.

In other words, bad genetics does not doom you to Alzheimer’s and dementia. A healthy lifestyle can cut your risk almost in half. Conversely, good genetics is not a “Get Out of Jail Free” card. You can squander the advantage of good genetics with an unhealthy lifestyle.

Simply put, both genetics and lifestyle influence the risk of developing Alzheimer’s Disease and dementia. However, the take-home lesson from this study is that:

  • A healthy lifestyle can partially offset the effect of bad genetics.
  • A healthy lifestyle can enhance the effect of good genetics.
  • An unhealthy lifestyle can negate the benefit of good genetics.

 

Can Lifestyle Overcome Genetics?

 

lifestyle over geneticsThis study clearly suggests that a healthy lifestyle can significantly reduce the effect of “bad” genetics on your risk of developing Alzheimer’s and other forms of dementia as you age. Considering that the medical profession has no other answer for preventing or treating Alzheimer’s Disease, this is really good news.

In the words of Dr. John Haaga of the U.S. National Institute on Aging: “No one can guarantee you’ll escape this awful disease, but you can tip the odds in your favor with clean living.”

The main strength of this study is its very large size. It is also supported by many smaller studies that have come to similar conclusions.

Moreover, a recent intervention study has been performed in Scandinavia in which one group was enrolled in a healthy lifestyle program while the other group continued with their previous health habits. That study also concluded that healthy habits could help prevent mental decline. The Alzheimer’s Association also has a similar intervention study in the United States. We should have more definitive information on this important subject very soon.

Finally, Alzheimer’s Disease may not be unique. Another recent study found that a healthy lifestyle can partially overcome a high genetic risk for developing heart disease.

 

The Bottom Line

 

A recent study looked at the effect of genetics and lifestyle on developing Alzheimer’s Disease and other forms of dementia. Here are the results from the study:

  • People at high genetic risk were almost twice as likely to develop dementia as those at low genetic risk.

In other words, genetics matter. If you have “bad” genes, your risk of developing dementia is increased significantly.

  • A healthy lifestyle decreased the risk of developing dementia by about 40% for both people at high genetic risk and for people at low genetic risk.

In other words, lifestyle also matters. You can significant decrease your risk of developing dementia, no matter what your genetic risk.

  • People at high genetic risk and an unhealthy lifestyle were almost three times more likely to develop dementia than people at low genetic risk and a healthy lifestyle.

In other words, the combination of a high genetic risk and an unhealthy lifestyle is the worst of all possible worlds.

  • People at low genetic risk and an unhealthy lifestyle were just as likely to develop dementia as people at high genetic risk and a healthy lifestyle.

In other words, bad genetics does not doom you to Alzheimer’s and dementia. A healthy lifestyle can cut your risk almost in half. Conversely, good genetics is not a “Get Out of Jail Free” card. You can squander the advantage of good genetics with an unhealthy lifestyle.

In the words of Dr. John Haaga of the U.S. National Institute on Aging: “No one can guarantee you’ll escape this awful disease, but you can tip the odds in your favor with clean living.”

For more details on the study and how a healthy lifestyle was defined in this study, 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 NOT follow this link or you will be banned from the site!