Coronary Heart Disease : New Research Blames Sugar and Exonerates Saturated Fat

For the past 60+ years, doctors have been telling us that saturated fat is responsible for the high number of people dying from coronary heart disease.

These recommendations have been largely based on the observational studies conducted by American scientist Dr. Ancel Keys. In his research, Dr. Keys observed that people who ate higher levels of saturated fat were prone to elevated serum cholesterol and were more likely to expire due to coronary heart disease.

Around the same time that Dr. Keys was presenting his research, another scientist, Dr. John Yudkin, came to a different conclusion – that it was excessive consumption of processed sugars that was driving the increase in coronary heart disease.

And for the next 60 years, both hypotheses have been defended with a succession of studies that:

  1. Observed what people ate
  2. Hypothesized which aspect of that complex diet of carbohydrates, protein, fats, enzymes, vitamins, minerals, etc was responsible for causing coronary heart disease

Unfortunately for us “normal people” who are looking to ways to live longer & better, this kind of science is pretty darn sketchy. Here’s why:

If you have pizza for dinner tonight, Dr. Keys would tell you that the saturated fat found in the cheese & pepperoni is bad for your heart. Conversely, Dr. Yudkin would blame the processed flour used to make the pizza crust.

So…who’s right?

If we rely on observational studies to answer this question, we will never come to a consensus. People don’t eat individual nutritional components…we eat FOOD. We eat meals in which we mix carbs and fats and proteins together.

Observational studies do nothing to separate those components and because of this…this kind of study is next to useless.

Luckily for us health-nerds, in the past fifty years, researchers have added to the observational studies with a giant body of research employing basic science, epidemiology and clinical trial data to provide us with a clearer picture of the relationship between nutrition and CHD risk, CHD events and CHD mortality.

And in their new study, Drs. DiNicolantonio, O’Keefe & Lucan have analyzed the best of that research and concluded that:

  • Saturated fat can raise levels of total serum cholesterol (TC) but TC is only modestly associated with coronary heart disease (CHD) and that some types of saturated fat are actually protective against CHD.
  • Conversely, when saturated fats are replaced with refined carbohydrates, and specifically with added sugars, we see increases in low-density lipoproteins (LDL), increases in triglycerides and decreases in high-density lipoproteins (HDL) that are shown to increase your odds of CHD.

Additionally, diets high in sugar may induce many other abnormalities associated with elevated CHD risk, including elevated levels of glucose, insulin, and uric acid, impaired glucose tolerance, insulin and leptin resistance, non-alcoholic fatty liver disease, and altered platelet function.

Does this mean that all sugars / carbs are bad?

NO, because while the body of research indicates that “a diet high in added sugars has been found to cause a 3-fold increased risk of death due to cardiovascular disease”, that doesn’t mean that all sugar/carbs are created alike.

Like some saturated fats are cardio-protective, we know that natural sugars found in whole fruits, grains and vegetables are not causing coronary heart disease.

It’s the processed fructose-containing sugars like sucrose and high-fructose corn syrup found in highly processed junk foods that are the problem.

 

 

For a more detailed look at the research, check out the link below.

Reference

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Childhood Obesity Leads to Heart Disease

Dutch researchers have found that 2/3 of severely obese children (aged 2–18 yrs) have been diagnosed with at least one cardiovascular risk factor:

  • 56% of the kids had hypertension,
  • 14% had high blood glucose,
  • 0.7% had type 2 diabetes,
  • 54% had low HDL-cholesterol

Even scarier….62% of severely obese children aged ≤12 years already had one or more cardiovascular risk factors.

Study Highlights

  • The definition of severe obesity started at a body mass index (BMI) of 20.5 for a 2 year old, at 31 for a 12 year old, and at 35 for an 18 year old.
  • Only one child’s obesity was attributable to medical rather than lifestyle factors.
  • Nearly one in three severely obese children came from one parent families.

Study Conclusion

“The prevalence of impaired fasting glucose in these children is worrying, considering the increasing prevalence worldwide of type 2 diabetes in children and adolescents,” write the authors. “Likewise, the high prevalence of hypertension and abnormal lipids may lead to cardiovascular disease in young adulthood,” they add. And they conclude: “Internationally accepted criteria for defining childhood obesity and guidelines for early detection and treatment of severe childhood obesity and underlying ill health are urgently needed.”

My Conclusion

Childhood obesity isn’t cute… and parents who enable it are doing their kids a HUGE disservice. 

 

Reference

You Are What Your Father Ate

Attention all fathers to be!!!

Researchers from the U of Mass have found that the food you eat is going to make a big difference upon the health of your future children.

So, before you inhale another bucket of popcorn chicken, be aware that your diet will influence the genetic makeup of your children.

In the UMass study, researchers found that adult mice fed a low protein diet produced offspring with an increase in the production of cholesterol synthesis genes.

And while this doesn’t mean that the wee baby mice are doomed to a lifetime of high cholesterol and prescriptions for lipitor, it does mean that a parent’s diet has a big impact on their kids –  in the form of changed epigentic information.

In the UMass experiment, scientists fed two different diets to two different groups of male mice – a standard diet and a low-protein diet. All females were fed a standard diet.

And as nature took it’s course and little mice babies were born, the researchers observed that the low-protein offspring showed an increase in the genes responsible for lipid & cholesterol production in comparison to the standard diet mice.

The observations are consistent with two human studies (1 & 2) which showed that a poor adolescent diet in one generation resulted in an increased risk of diabetes, obesity and cardiovascular disease in second-generation offspring.

However, since these previous human studies were retrospective and involved dynamic populations, they were unable to completely account for all social and economic variables.

Hence this study with lab mice.

According to lead researcher Oliver Rando, “Our study begins to rule out the possibility that social and economic factors, or differences in the DNA sequence, may be contributing to what we’re seeing. It strongly implicates epigenetic inheritance as a contributing factor to changes in gene function.”

Co-author Hans Hofmann continues by saying that “the results also have implications for our understanding of evolutionary processes. It has increasingly become clear in recent years that mothers can endow their offspring with information about the environment, for instance via early experience and maternal factors, and thus make them possibly better adapted to environmental change. Our results show that offspring can inherit such acquired characters even from a parent they have never directly interacted with, which provides a novel mechanism through which natural selection could act in the course of evolution.”

So, what does this mean?

According to Dr. Rando, “we often look at a patient’s behavior and their genes to assess risk. If the patient smokes, they are going to be at an increased risk for cancer. If the family has a long history of heart disease, they might carry a gene that makes them more susceptible to heart disease. But we’re more than just our genes and our behavior. Knowing what environmental factors your parents experienced is also important.”

What’s next for this research?

Drs. Rando et al will begin to explore how and why this genetic reprogramming is being transmitted from generation to generation. “We don’t know why these genes are being reprogrammed or how, precisely, that information is being passed down to the next generation,” said Rando. “It’s consistent with the idea that when parents go hungry, it’s best for offspring to hoard calories, however, it’s not clear if these changes are advantageous in the context of a low-protein diet.”

What does this mean for you?

It means that not only will that bucket of popcorn chicken screw up your health, it will probably screw up your kid’s health as well.

Reference

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Beets Lower Blood Pressure

Last summer, I told you about an interesting study that showed that drinking beet root juice boosts your stamina and could help you exercise for up to 16% longer.

At that time, the theory was that the nitrate contained in beet root juice leads to a reduction in oxygen uptake, making exercise less tiring.

Beetroot Juice

The researchers weren’t sure of the exact mechanism that caused the nitrate in the beet root juice to boost stamina, but they suspected that it could be a result of the nitrate turning into nitric oxide in the body, reducing the oxygen cost of exercise.

And they were right.

In a study published today, researchers were able to demonstrate that the nitrate found in beetroot juice was in fact the cause of its beneficial effects upon cardiovascular health by increasing the levels of the gas nitric oxide in the circulation.

And it goes beyond improving athletic performance.

According to the research, test subjects who consumed either 250 ml of beetroot juice or an equivalent inorganic nitrate supplement were able to lower their blood pressure within 24 hours. And considering that cardiovascular disease is the world’s biggest killer, having a natural solution to hypertension is pretty damn awesome.

Reference

 

 

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The Link between Belly Fat, Depression, Diabetes and Cardiovascular Disease

sad homer
sad homer

In a previous article, I wrote about the link between belly fat (visceral fat) and depression.

I have also written numerous articles on the links between belly fat and chronic disease:

Today’s post connects all of that research.

Today’s post is based on the findings of this study, which suggest that belly fat (visceral fat) “is an important pathway by which depression adds to the risk for cardiovascular disease and diabetes.”

The Study

fat
Visceral belly fat is the white stuff surrounding your organs. Subcutaneous fat is the white stuff on top of the muscles but under the skin

Researchers from Rush University Medical Center looked at over 400 women “who were participating in the Women in the South Side Health Project (WISH) in Chicago, a longitudinal study of the menopausal transition”.

They screened the women for depression and measured their visceral fat with a CT scan.

Even after adjusting for variables that might account for the accumulation of visceral fat, the researchers found a strong correlation between depression and high levels of visceral fat.

The women who showed signs of depression (assessed using the CES-D scale) had 24.5% more visceral belly fat than the women with fewer depressive symptoms.

No association was found between depression and subcutaneous belly fat (non-visceral).

So, what does this mean and why is depression linked to increased visceral fat, diabetes and cardiovascular disease?

Lead researcher Dr. Lynda Powell speculated that “depression triggers the accumulation of visceral fat by means of certain chemical changes in the body”.

Some of those changes could include:

Future studies are planned to address the specific glucocorticoid or inflammatory mechanisms responsible for the link between depression, visceral body fat, diabetes and cardiovascular disease.

But for now, it’s going to have to be good enough to simply know that the link exists.

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