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Friday, April 19, 2024
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New research has found that short bursts of exercise may significantly improve levels of metabolites that are indicators of key physical health issues.

The research, published in the journal Circulation, offers scientists a better understanding of the beneficial effects exercise can have on a person’s health.

Health and physical activity

Scientists have known for a long time that there is a link between physical activity and better health. As the Centers for Disease Control and Prevention (CDC) say, “Regular physical activity is one of the most important things you can do for your health.”

The CDC note that regular exercise can improve a person’s brain health; help them better manage their weight; reduce their chances of developing various diseases, including diabetes, some cancers, and cardiovascular disease; strengthen their muscles and bones; and improve mental health.

While scientists are well aware of these links, they do not fully understand the precise molecular mechanisms that help explain the link between being physically active and maintaining better health.

Metabolites

In this context, the researchers wanted to look at the association between metabolites that are indicators of health and exercise.

A person’s metabolism describes the chemical reactions that take place in their body. Metabolites either facilitate these reactions or are the end result of them. Scientists have identified relationships between exercise and certain changes in metabolites.

Dr. Gregory Lewis, section head of Heart Failure at Massachusetts General Hospital (MGH) and senior author of the study, says, “Much is known about the effects of exercise on cardiac, vascular, and inflammatory systems of the body, but our study provides a comprehensive look at the metabolic impact of exercise by linking specific metabolic pathways to exercise response variables and long-term health outcomes.”

He continues:

“What was striking to us was the effects a brief bout of exercise can have on the circulating levels of metabolites that govern such key bodily functions as insulin resistance, oxidative stress, vascular reactivity, inflammation, and longevity.”

Burst of exercise

The researchers made use of the Framingham Heart Study (FHS), a long-term study directed by the National Heart, Lung, and Blood Institute.

The researchers measured 588 metabolites in 411 middle-aged people before and immediately after 12 minutes of physical activity on an exercise bike. This allowed them to see the effect that exercise has on the metabolome.

In general, the researchers found that the short burst of exercise significantly altered 80% of a participant’s metabolites. In particular, they found that metabolites associated with adverse health outcomes when resting were reduced.

For example, high levels of glutamate have been linked to diabetes, heart disease, and hypertension, and the researchers found that these levels fell by 29% following exercise. The levels of dimethylguanidine valerate (DMGV), which are associated with liver disease and diabetes, fell by 18% following exercise.

Marker of fitness?

The researchers note that their findings may be valuable in helping doctors determine a person’s fitness levels.

Dr. Matthew Nayor, a cardiologist in the Heart Failure and Transplantation section of the MGH Cardiology Division, explains, “Intriguingly, our study found that different metabolites tracked with different physiologic responses to exercise, and might therefore provide unique signatures in the bloodstream that reveal if a person is physically fit, much the way current blood tests determine how well the kidney and liver are functioning.”

He adds, “Lower levels of DMGV, for example, could signify higher levels of fitness.”

By combining the information they gained from this analysis with blood samples taken during previous rounds of the FHS, the researchers were also able to determine the longer-term effects of exercise on a person’s metabolome.

Dr. Ravi Shah of the Heart Failure and Transplantation section of the MGH Cardiology Division notes, “We’re starting to better understand the molecular underpinnings of how exercise affects the body and use that knowledge to understand the metabolic architecture around exercise response patterns.”

He adds, “This approach has the potential to target people who have high blood pressure or many other metabolic risk factors in response to exercise, and set them on a healthier trajectory early in their lives.”

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A clinical trial has found that a monoclonal antibody reduces low-density lipoprotein (LDL) cholesterol levels by 50% in people with an inherited condition called familial hypercholesterolemia.

Individuals with high levels of low-density lipoprotein (LDL) or “bad” cholesterol in their blood are at increased risk of developing atherosclerosis (narrowed arteries) and cardiovascular disease.

Doctors define severe hypercholesterolemia as untreated LDL cholesterol levels of at least 190 milligrams per deciliter (mg/dl) of blood.

Cardiologists in the U.S. recommend that individuals who are at very high risk of cardiovascular disease due atherosclerosis aim for an LDL cholesterol level of around 70 mg/dl of blood.

Lifestyle changes can help reduce LDL, but people usually need to take cholesterol-lowering drugs to reach this goal. In addition, certain genetic differences can make achieving this objective more difficult for some people.

Worldwide, approximately 1 in 250 adults have an inherited condition called heterozygous familial hypercholesterolemia. This usually results from mutations in a gene for a receptor that removes LDL from the bloodstream.

Doctors usually prescribe a standard “triple therapy” of three types of cholesterol-lowering drugs for hypercholesterolemia:

  • A high dose of a statin, which reduces the amount of cholesterol the body produces.
  • A PCSK9 inhibitor, which boosts the number of LDL receptors in the liver.
  • Ezetimibe, which limits the absorption of cholesterol from the intestine.

For individuals whose LDL cholesterol level remains too high despite taking the maximum tolerable dose of this drug combination, a new drug called evinacumab that acts on a different target may soon be available.

A clinical trial published in The New England Journal of Medicine suggests that evinacumab could further reduce LDL levels in these individuals by around 50%.

This would be good news for people with mutations in the gene for the LDL receptor who don’t respond particularly well to PCSK9 inhibitors.

“There’s an unmet need for agents that address refractory hypercholesterolemia through a pathway that’s independent of the LDL receptor,” explains principal investigator Robert Rosenson, MD, Director of Cardiometabolic Disorders at the Icahn School of Medicine at Mount Sinai in New York, N.Y.

“If approved by the U.S. Food and Drug Administration, evinacumab may potentially fill that clinical gap for patients by reducing severely elevated LDL cholesterol,” he adds.

Breaking down lipids

Evinacumab is a monoclonal antibody that targets a protein called angiopoietin-like 3 (ANGPTL3). Normally, ANGPTL3 inhibits enzymes that break down lipids, including LDL, high-density lipoprotein (HDL), and triglycerides.

People with a faulty version of the gene that makes ANGPTL3 have abnormally low levels of these lipids in their blood. As a result, their chance of developing coronary artery disease is 41% lower than the general population.

By disabling ANGPTL3 with an antibody, drug developers hoped to recreate these beneficial effects in people with very high cholesterol levels.

In this phase II clinical trial, the researchers randomly assigned 272 people to receive either evinacumab — through intravenous or subcutaneous administration at various doses — or placebo treatments.

Most of the participants had heterozygous familial hypercholesterolemia.

After 16 weeks, LDL cholesterol had fallen by an average of 56% compared with placebo in those who received a subcutaneous dose of 450 mg of evinacumab weekly.

Among those who received a monthly intravenous injection of 15 mg evinacumab per kilogram of body weight, LDL cholesterol fell by 50.5% compared with the placebo group.

The authors note that some people prefer subcutaneous administration because they can do it themselves at home, avoiding the need to take time off work to visit a clinic.

Commenting on the findings, Dr. Rosenson concludes:

“Our study demonstrates that a regimen of either subcutaneous or intravenous evinacumab can have a significant impact on LDL cholesterol […] If approved for use in this setting, evinacumab could potentially arm cardiologists with a major new add-on therapy to bring patients with [heterozygous familial hypercholesterolemia] to or closer to their cholesterol-lowering goal.”

Racial diversity

The authors concede that their study had some limitations. For example, the numbers in each arm of the study were relatively small, and treatment lasted only 16 weeks.

In addition, the racial diversity of participants was not as broad as the researchers had hoped, so the results may not apply to all people in the wider population.

One of the people treated with subcutaneous evinacumab had difficulty breathing, and another had a mild anaphylactic reaction.

The pharmaceutical company Regeneron, which makes evinacumab, sponsored the study.

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A recent study reveals that losing fat without reducing muscle mass results in a significantly lower risk of heart failure in people with type 2 diabetes.

In the United States, around 1 in 10 people have diabetes, and 90–95% of them have type 2 diabetes. Type 2 diabetes usually develops after age 45. Estimates suggest that by 2045, 700 million adults worldwide will have this condition.

Type 2 diabetes usually begins as insulin resistance. This is a condition wherein the body’s cells no longer react to the insulin the pancreas produces to control blood sugar.

Genetics, ethnicity, and advancing age all play a role in the development of insulin resistance and diabetes. However, excess weight, a lack of exercise, an unhealthful diet, and smoking may be driving factors in its occurrence.

Once doctors diagnose this condition, the primary treatments they advise generally include taking medications and making certain lifestyle changes, such as losing weight and improving the diet.

As diabetes nearly doubles the risk of death due to heart disease or stroke and increases the risk of having heart failure by a factor of two in males and five in females, many researchers are focusing on preventing these and similar health complications for those with diabetes.

Heart failure, or congestive heart failure, occurs when the heart muscle does not pump the blood adequately. This leads to a buildup of fluid in the lungs or legs, or sometimes both.

Heart failure has a number of potential causes. For example, after a heart attack (when the heart muscle sustains damage due to a lack of oxygen), the muscle is weak and cannot pump well.

Heart failure can also occur due to type 2 diabetes. This is as a result of direct harm to the heart muscle from raised blood sugar and systemic inflammation associated with the condition.

One prevention strategy includes weight loss for people with overweight or obesity. However, not much is known regarding what type of weight loss has the most impact on reducing the risk of diabetes-related heart issues.

The study

To investigate this further, researchers at the University of Texas Southwestern Medical Center (UTSW) in Dallas analyzed data from the Look AHEAD study.

This is a randomized trial investigating weight loss due to intensive lifestyle intervention, consisting of healthful eating and increased physical activity versus support and education alone in people with type 2 diabetes.

The UTSW research, which appears in the journal Circulation, received funding from the National Heart, Lung, and Blood Institute, the Texas Health Resources Clinical Scholars Program, and the National Institutes of Health (NIH).

The researchers selected 5,103 people from the Look AHEAD study who did not have heart failure at the beginning of the study. The participants also had sufficient baseline measurements needed for prediction equations to estimate how much fat mass and lean (muscle) mass they had.

Data on the participants’ weight and waist circumference were available at the beginning of the study and over a 4-year period. The team also noted hospitalizations for heart failure over a 12-year time frame.

During the trial’s 12-year follow-up, 257 study participants were hospitalized for heart failure treatment.

In the Look AHEAD study, scientists used a scanning technique called dual-energy X-ray absorptiometry (DXA) to determine body composition in a subset of about 1 in 5 of the participants. These participants also had information recorded on factors such as height, weight, waist circumference, and ethnicity.

This meant that the researchers could validate existing equations that predict the proportion of fat mass and lean mass from these factors, which are simple to collect compared with the much more complicated process of conducting a DXA scan.

The researchers’ analysis of the subset of participants with DXA scans provided a new equation specific to this study group. They applied this new equation to the remaining participants without a DXA scan to accurately predict their fat mass and lean mass.

This revealed that adults in the study who had lost weight were less likely to develop heart failure if they lowered their fat mass and waist circumference. However, losing lean mass did not change their risk.

The investigators note that although the risk of heart failure decreased in those who lost body fat and reduced their waist circumference, the study data showed no significant reductions in heart attack risk.

The team also considered the participants’ ejection fraction (EF) ratio. This is a measurement of the amount of blood leaving the heart with each contraction.

The data showed that reducing body fat mass by 10% resulted in a 22% lower risk of heart failure with preserved EF ratio and a 24% lower risk of heart failure with reduced EF ratio.

“Our study suggests that simply losing weight is not enough. We may need to prioritize fat loss to truly reduce the risk of heart failure.” – Study co-author Dr. Kershaw Patel, a cardiologist at Houston Methodist Hospital in Texas

Supporting evidence

A study from May this year, which appears in the journal Circulation Research, compared obesity phenotypes, diabetes, and cardiovascular diseases.

The comparison suggests that some people who have a healthy weight or overweight but an excess amount of fat deposits around the internal organs and under the skin have a higher risk of diabetes and heart disease.

The researchers say that it is not possible to determine the risk of cardiovascular disease and type 2 diabetes based on body mass index (BMI) alone — mostly because body composition is so diverse.

They suggest that since excessive amounts of fat tissue largely define cardiovascular risks, reducing body fat is critical for prevention.

Implications and limitations

The results of the UTSW study suggest that for people with diabetes who also have overweight, losing weight, in general, may not be adequate to reduce heart health risks.

If further studies replicate these findings, it could confirm that losing weight by shedding visceral fat from around the organs — rather than losing muscle mass — is a key factor when it comes to reducing the risk of heart failure in type 2 diabetes.

The study authors also say that further investigation is necessary to determine if building or maintaining muscle in addition to losing fat mass would be even more effective in reducing the risk of diabetes-related heart failure.

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A high fat, low carb diet reversed heart failure in a mouse model of the condition. A 24-hour fast also led to improvements, mimicking the physiological effects of the diet.

In people with heart failure, the muscle on the right or left side of the heart — or on both sides — weakens. This impairment limits the organ’s ability to pump blood around the body, causing fatigue and shortness of breath, among other symptoms.

The leading causes are high blood pressure, diabetes, and ischemic heart disease, in which the heart muscle becomes starved of oxygen.

The National Heart, Lung, and Blood Institute estimate that about 5.7 million people in the United States have heart failure.

There is currently no cure, but medications and lifestyle changes can improve people’s quality of life and increase their lifespan.

Healthy heart muscle can draw upon a variety of chemical energy sources, depending on the circumstances. One of these is a molecule called pyruvate, which the body generates during the breakdown of the sugar glucose.

However, conditions such as heart failure and diabetes reduce this flexibility, starving the muscle of the fuel it needs to function effectively.

Fuel shuttle

Researchers have now traced this loss of flexibility to a transporter protein that shuttles pyruvate into mitochondria — the so-called power stations of cells.

Known as the mitochondrial pyruvate carrier (MPC) complex, it comprises two subunits: MPC1 and MPC2.

Researchers at the Saint Louis University School of Medicine in St. Louis, MO, led a team who discovered that the production of both subunits is reduced in failing human hearts.

The researchers compared heart tissue samples from people undergoing heart surgery with tissue samples from donor hearts that were healthy but unsuitable for transplant.

They then showed that mice that lack the gene for producing MPC2 steadily develop heart failure over time. Their hearts became outsized, or hypertrophied, and the organs’ ability to pump blood diminished.

Crucially, the scientists found that they could reverse the damage to the animals’ heart muscle by simply feeding them a special diet for 3 weeks.

“Interestingly, this heart failure can be prevented or even reversed by providing a high fat, low carbohydrate ‘ketogenic’ diet,” explains Kyle S. McCommis, Ph.D., assistant professor of biochemistry and molecular biology at the university, who led the research.

“A 24-hour fast in mice, which is also ‘ketogenic,’ also provided significant improvement in heart remodeling,” he adds.

Ketogenic diet

The ketogenic diet has been growing in popularity in recent years, with research suggesting that it has a range of possible health benefits. These include supporting weight loss, improving heart health, and preventing seizures in some types of epilepsy.

By severely restricting the intake of carbohydrates, such as glucose and other sugars and starches, the diet forces the body to break down fat, producing molecules called ketones that it can use as fuel. Intermittent fasting may achieve similar effects, though adhering to the regimen can be challenging.

The new research indicates that a ketogenic diet promotes the breakdown of fatty acids in heart muscle cells. This process produces an alternative fuel called acetyl-CoA, which the mitochondria can use as an energy source instead of pyruvate.

“Thus, these studies suggest that consumption of higher fat and lower carbohydrate diets may be a nutritional therapeutic intervention to treat heart failure,” says McCommis.

The scientists showed that the diet reversed heart failure by promoting the breakdown of fatty acids in mitochondria rather than ketones. Supplying the mitochondria with extra ketones only slightly improved heart failure.

Converging evidence

The findings from this study appear in the journal Nature Metabolism.

Two studies by other research groups, which feature in the same issue, independently show that the MPC transporter protein plays a central role in heart failure.

P. Christian Schulze and Jasmine M. F. Wu, who are both cardiologists from the University Hospital Jena in Germany, have written a comment article for the journal about the three papers.

While several questions remain unanswered about the regulation of MPC levels in healthy and failing hearts, they conclude:

“The current findings suggest a role for specific ketogenic diets as a supportive, nonpharmacologic treatment in people with heart failure.”

The cardiologists speculate that the findings could also inspire the development of new drugs for heart failure that work by boosting the breakdown of fatty acids in heart muscle cells.

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Researchers have discovered an imbalance in the amounts of fatty molecules called lipids inside the brain cells of people with Parkinson’s disease. A buildup of lipids in nerve cells may cause inflammation.

Parkinson’s disease is a movement disorder that gets progressively worse over time.

The death of dopamine-producing nerve cells in the substantia nigra region of the brain causes the illness. Dopamine is a neurotransmitter that plays several vital roles, including regulating motivation, reward, and movement.

However, the exact train of events leading to the death of dopamine-producing cells remains unclear.

Researchers have focused much of their attention on a misfolded form of a protein called alpha-synuclein as the trigger for Parkinson’s. Studies have found toxic clumps or aggregates of the misfolded protein in the brains of people with the disease.

However, an alternative theory proposes that lipid dysregulation and inflammation play a more important role, similar to the part played by fatty plaques and inflammation in the walls of arteries in cardiovascular disease.

Researchers at the Neuroregeneration Institute at McLean Hospital in Belmont, MA, have now discovered an accumulation of lipids in dopamine-producing neurons in the postmortem brains of people who had Parkinson’s.

The excess amounts of lipid in these nerve cells correlate with changes in lipid levels in neighboring cells called microglia and astrocytes. They also found evidence of inflammation.

When the researchers simulated a breakdown of lipid metabolism in an animal model of the disease, they saw remarkably similar changes.

“These results support our lipid-inflammation hypothesis in the causation of Parkinson’s disease initiation and progression,” says senior author Dr. Ole Isacson, who is the founding director of the Neuroregeneration Institute and a professor of neurology at Harvard Medical School in Boston, MA.

“[The results] may help us discover and develop new therapies by leaving behind conventional thinking about [Parkinson’s disease] pathology, which to some extent has been limited to neurons and protein aggregates,” he adds.

The study appears in the journal Proceedings of the National Academy of Sciences.

Postmortem tissue samples

The scientists compared postmortem brain tissue from 26 individuals with Parkinson’s with 23 age-matched controls without the disease.

They used fluorescent lipid-binding molecules to determine lipid levels in different brain cells in the substantia nigra.

In brain tissue from people with Parkinson’s, there was an accumulation of lipids inside dopamine nerve cells, which was matched by a deficiency of lipids within astrocytes in the same samples.

Astrocytes are star-shaped cells that support nerve cells, both structurally and through the exchange of nutrients and their byproducts.

In their paper, the researchers note that nerve cells have a limited capacity to use lipids for energy, with excess amounts being transported to neighboring astrocytes to avoid the buildup of toxic byproducts.

This did not seem to be happening correctly in the brains of individuals with Parkinson’s.

Compared with healthy brain tissue, the scientists also found excess amounts of lipid inside microglia, which are the brain’s immune cells.

They also discovered high levels of a signaling molecule called GPNMB. Scientists know that astrocytes produce this molecule in response to inflammation caused by the build up of lipids.

The scientists found that levels of this molecule correlated with the total amount of lipid in the brain tissue of individuals with Parkinson’s.

Mouse model of Parkinson’s

Finally, the scientists investigated whether they could reproduce these effects in mice by disrupting lipid metabolism in the animals’ brains.

One of the most significant genetic risk factors for Parkinson’s is a mutation in a gene for an enzyme that breaks down lipids.

When the researchers injected the mice with a chemical that inhibits this enzyme, they found the same pattern of changes in lipid distribution that they had seen in brain tissue from people with Parkinson’s.

Previous research has found telltale deposits of alpha-synuclein in mice injected with this enzyme inhibitor.

In their paper, the scientists conclude:

“Therapies and agents that reverse the pathological cell-type-specific lipid distribution in the [substantia nigra of people with Parkinson’s] could serve to prevent and reduce the progression of [Parkinson’s disease] and related neurodegenerative disorders.”

However, researchers need to carry out much more research to confirm the findings and translate them into effective and safe treatments.

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In celebration of this year’s World Heart Day, Wella Health, a leading African health tech startup, is carrying out free blood pressure tests for over 100,000 Nigerians across its 600 partner pharmacies from Tuesday September 29 to October 29 this year.

World Heart Day is observed and celebrated every September 29. The global awareness day is intended to increase public understanding of cardiovascular diseases, prevention, early detection and treatment.

According to research, cardiovascular diseases commonly referred to as CVDs are the number one cause of death globally, killing 17.9 million people yearly and accounting for 31 per cent of all global deaths.

Speaking on the campaign, CEO Wella Health, Dr Neto Ikpeme stated that cardiovascular diseases are often perceived as a problem strictly for older people. “Unfortunately, it is now more common in adolescents and young adults.”

According to the expert, for 25 to 34-year-old men and women, heart disease is the fourth leading cause of death while for 35 to 44-year-olds, heart disease is even deadlier and is the second biggest killer of men and third biggest killer of women.

“CVDs can affect anyone and at any age. The rise in obesity and diabetes at earlier ages also adds to the overall risk,” he added.

By offering free blood pressure tests to over 100,000 Nigerians in celebration of world heart day and later world stroke day coming up in October, Ikpeme said their goal is to join the global fight against cardiovascular diseases and minimise mortality, especially among young adult.

In his perspective, a blood pressure screening is important because high blood pressure usually has no symptoms and cannot be detected without being measured.

He noted, “High blood pressure is the number one risk factor for heart disease and often considered a silent killer.”

Experts have revealed that the primary causes of cardiovascular diseases are smoking, unhealthy diet, physical inactivity and the harmful use of alcohol which in turn show up in people as high blood pressure, high blood sugar and obesity.

His words, “Lifestyle changes including healthy eating, regular physical activity and quitting tobacco use are advised to improve heart health.”

Wellahealth is a health technology startup focused on providing affordable and accessible high-quality healthcare protection for all Africans.

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A study in the United States demonstrates that mortality rates from heart failure are higher in counties where people face more poverty and social deprivation.

Heart failure, sometimes called congestive heart failure, is a chronic condition in which the heart is unable to pump enough blood around the body to meet its needs.

The condition is irreversible, although there are treatments that can help people live longer, more active lives.

About 5.7 million people in the U.S. have heart failure, according to the National Heart, Lung, and Blood Institute.

A new study suggests that the risk of dying from the condition is not spread evenly across the country, but that mortality rates are higher in poorer, more socially deprived areas.

Researchers at University Hospitals Cleveland Medical Center, OH, analyzed 1,254,991 deaths from heart failure across 3,048 counties between 1999 and 2018.

They used two standard indices of social deprivation: the Area Deprivation Index (ADI), which takes into account multiple local measures, including employment, poverty, and education, and the Social Deprivation Index (SDI), which is based on income and housing.

After adjusting for age, they found that the average death rate from heart failure per county was 25.5 deaths per 100,000 head of population.

However, counties with higher rates of socioeconomic deprivation had higher death rates from heart failure, and the association held up regardless of race or ethnicity, sex, and degree of urbanization.

The levels of deprivation that the ADI measures accounted for roughly 13% of the variability in heart failure mortality among counties. This scale of risk is similar to that of other recognized risk factors for heart failure, such as obesity and diabetes, say the scientists. Correlation with housing and income — the social factors that the SDI measures — accounted for 5% of this variability.

The study features in the latest issue of the Journal of Cardiac Failure.

Persistent inequality

The research revealed that the imbalance in survival rates between wealthy and deprived areas changed little between 1999 and 2018.

“Analysis of trends in heart failure mortality shows that these disparities have persisted throughout the last two decades,” says first author Dr. Graham Bevan, a resident physician at University Hospitals.

Bevan and his colleagues say that a range of factors may be responsible for the increased risk of dying from heart failure in poorer counties. These include reduced access to healthcare, substandard care, and poor health literacy.

They also note that the successful treatment of heart failure is dependent on patients adhering to a complex and often expensive drug regimen.

The authors write:

“Regardless of the contributing factors, the association between communities with high socioeconomic deprivation and [heart failure] mortality is strong and suggests that targeting social deprivation may be impactful in reducing [heart failure] mortality. Additionally, the yield of intensive [heart failure] preventive strategies may be higher in areas with high social deprivation.”

The American Heart Association (AHA) believe that aggressively tackling the major clinical risk factors for heart failure could significantly reduce the death toll. These clinical factors include hypertension, heart attacks, obesity, diabetes, and disorders of the heart valves.

“Living in a particular county should not mean you’re more likely to die from heart failure,” says co-author Dr. Sadeer G. Al-Kindi, a cardiologist at University Hospitals’ Harrington Heart and Vascular Institute.

“University Hospitals has a history of addressing healthcare disparities in underserved communities and, armed with the information from this study, we can thoughtfully create solutions to better serve these populations.”

One of the limitations of their study, the authors write, was that it relied on the information given on death certificates, which may not be accurate in every instance.

Also, the study was not designed to tease apart the effects of other recognized risk factors for heart failure mortality, some of which — such as lack of physical activity, obesity, diabetes, and high blood pressure — may also be associated with poverty. However, a recent study showed that these factors together failed to account for 57% of the geographical variation in deaths from heart failure among counties in the U.S.

This new study suggests that socioeconomic deprivation may help explain part of that variation.

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A study links the consumption of ultra-processed foods with the shortening of the body’s telomeres.

Telomeres are structures located at the ends of our chromosomes. Although they contain no genetic information themselves, they preserve the integrity of chromosomes by keeping their ends from fraying, much as shoelace tips protect the laces.

Telomeres become shorter and less effective over time as chromosomes replicate. Scientists view them as markers of an individual’s biological age at a cellular level.

New research indicates that eating ultra-processed foods is linked to the accelerated shortening of telomeres and cell aging.

The researchers, from the University of Navarra in Pamplona, Spain, presented their findings at this year’s European and International Congress on Obesity (ECOICO 2020) in September.

The findings also feature in a study paper in The Americal Journal of Clinical Nutrition.

Lucia Alonso-Pedrero, who is a doctoral researcher at this university, led the study.

The rise of ultra-processed foods

The consumption of ultra-processed foods, or UPFs, is on the rise worldwide. UPFs are manufactured food products comprising the building blocks of naturally occurring foods: protein isolates, sugars, fats, and oils.

However, while their components are often extracted from natural sources, UPFs ultimately contain no, or very little, in the way of whole foods.

The companies that produce UPFs often add flavorings and emulsifiers for taste, as well as colorings and other cosmetic additives to achieve the desired appearance. UPFs are nutritionally poor and often unbalanced.

UPFs are highly profitable for their producers due to their inexpensive ingredients, cost effective manufacturing processes, and long shelf life in stores. What makes them so attractive to consumers is their convenience and their relative imperishability.

Previous research has not conclusively established a link between UPFs in general and telomere length (TL). However, researchers have noted associations between TL and alcohol, sugar-sweetened beverages, processed meats, and foods high in saturated fat and sugar.

Other research indicates a UPF connection to several serious conditions, such as obesity, hypertension, depression, metabolic syndrome, some types of cancer, and type 2 diabetes. However, these conditions also tend to be age-related and thus difficult to associate definitively with the consumption of UPFs.

UPFs and telomere length

The NOVA system classifies foods according to the degree of processing that their production involves, as opposed to their nutritional content. The goal of Alonso-Pedrero and her colleagues was to investigate the effect of UPF consumption in older adults using NOVA as a means of categorizing the foods that they consumed.

The researchers began their analysis with data from the SUN project, which the University of Navarra is conducting with other Spanish universities. The ongoing study began recruiting in 2000 and includes volunteers over the age of 20 years. Participants are required to fill out and return questionnaires every 2 years.

In 2008, all SUN participants over the age of 55 years took part in a genetic study that forms the foundation of the new research. A total of 886 individuals — 645 men and 241 women — provided saliva samples for DNA analysis and self-reported their daily food consumption. Their average age was 67.7 years.

The team sorted the participants into four groups of equal size, or quartiles, according to the number of UPF servings that they consumed daily:

  • low: under 2 servings
  • medium-low: 2–2.5 servings
  • medium-high: 2.5–3 servings
  • high: more than 3 servings

In terms of telomeres, Alonso-Pedrero and her colleagues detected a clear correspondence between TL and the consumption of UPFs.

The likelihood of shortened telomeres increased dramatically with the number of UPF servings, starting with the medium-low group. That group was 29% more likely to exhibit reduced TL, while the medium-high group was 40% more likely to do so. Those in the high group were 82% more likely to have shortened telomeres.

The study’s authors write:

“In this cross-sectional study of elderly Spanish subjects, we showed a robust strong association between UPF consumption and TL. Further research in larger longitudinal studies with baseline and repeated measures of TL is needed to confirm these observations.”

The researchers also made a number of general observations regarding those who consumed more than 3 servings of UPFs per day. People in this quartile:

  • were more likely to have diabetes, a family history of cardiovascular disease, and abnormal blood fats under their skin
  • were the participants most likely to snack between meals
  • consumed less protein, carbohydrate, fiber, fruit, vegetables, olive oil, and other micronutrients

Individuals who ate more UPFs were less likely to adhere to a healthful Mediterranean diet. In exchange, they consumed more fats, saturated fats, polyunsaturated fats, sodium, sugar-sweetened beverages, cholesterol, fast food, and processed meats.

The study authors also found that those who consumed higher amounts of UPFs were more likely to experience depression — especially when they were less active physically.

Finally, the findings linked the consumption of UPFs to excessive body weight, hypertension, and all-cause mortality.

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If your cholesterol level has crept up over the years, you may wonder whether changing your diet can help. Ideally, your total cholesterol value should be 200 milligrammes per deciliter (mg/dL) or lower. But it is the harmful Low-Density Lipo-protein (LDL) ‘bad’ cholesterol value that experts worry about the most. Excess LDL builds up on artery walls and triggers a release of inflammatory substances that boost heart attack risk.

“To prevent heart disease, your LDL should be 100 mg/dL or lower,” says Dr. Jorge Plutzky, director of preventive cardiology at Harvard-affiliated Brigham and Women’s Hospital. But many Americans have LDL values that are less than optimal (100 to 129 mg/dL) or borderline high (130 to 159 mg/dL).

If you fall into either of those categories, you may be able to nudge down your LDL to a healthier level by changing what you eat, particularly if your current diet could use some improvement. However, most people with higher LDL values likely will also need to take a cholesterol-lowering drug, such as a statin, says Dr. Plutzky.

Dietary directives
Avoiding foods that are high in cholesterol isn’t the best way to lower your LDL. Your overall diet — especially the types of fats and carbohydrates you eat — has the most impact on your blood cholesterol values. “As the American Heart Association has noted, you’ll get the biggest bang for your buck by lowering saturated fat and replacing it with unsaturated fat,” says registered dietitian Kathy McManus, director of the Department of Nutrition at Brigham and Women’s Hospital.

That means avoiding meat, cheese, and other high-fat dairy products such as butter, half-and-half, and ice cream. Equally important is replacing those calories with healthy, unsaturated fats (such as those found in vegetable oils, avocados, and fatty fish) rather than refined carbohydrates such as white bread, pasta, and white rice. Unlike healthy fats, these starchy foods aren’t very filling, and they can trigger overeating and weight gain.

The other big problem with refined carbs: They are woefully low in fibre, which helps flush cholesterol out of the body.

The fibre factor
Your body can’t break down fiber, so it passes through your body undigested. It comes in two varieties: insoluble and soluble. Fiber-containing foods usually feature a mix of the two.

Insoluble fibre does not dissolve in water. While it doesn’t directly lower LDL, this form of fiber fills you up, crowding other cholesterol-raising foods out of your diet and helping to promote weight loss.

Soluble fibre dissolves in water, creating a gel. This gel traps some of the cholesterol in your body, so it’s eliminated as waste instead of entering your arteries.

Soluble fibre also binds to bile acids, which carry fats from your small intestine into the large intestine for excretion. This triggers your liver to create more bile acids — a process that requires cholesterol. If the liver doesn’t have enough cholesterol, it draws more from the bloodstream, which in turn lowers your circulating LDL.

Finally, certain soluble fibres (called oligosaccharides) are fermented into short-chain fatty acids in the gut. These fatty acids may also inhibit cholesterol production.

The “best” foods
The following 11 foods are good sources of fibre or unsaturated fat (or both). But they’re not in any particular order and are simply suggestions. Most whole grains, vegetables, and fruits are good sources of fiber. And most nuts and seeds (and the oils made from them) provide monounsaturated or polyunsaturated fats.

1. Oatmeal. This whole grain is one of the best sources of soluble fiber, along with barley (see “Grain of the month,” at right). Start your day with a bowl of steel-cut or old-fashioned rolled oats, topped with fresh or dried fruit for a little extra fiber.

2. White beans. Also called navy beans, this variety ranks highest in fiber content. Try different types of beans as well, such as black beans, garbanzos, or kidney beans, which you can add to salads, soups, or chili. But avoid prepared baked beans, which are canned in sauce that’s loaded with added sugar.

3. Avocado. The creamy, green flesh of an avocado is not only rich in monounsaturated fat; it also contains both soluble and insoluble fiber. Enjoy this fruit sliced in salad, pureed into dip, or mashed and spread on a slice of whole-grain toast.

4. Eggplant. Although not everyone’s favorite, these deep purple vegetables are one of the richest sources of soluble fiber. One idea: oven-roast or grill whole eggplants until soft and use the flesh in a Middle Eastern dip called baba ghanoush.

5. Carrots. Raw baby carrots are a tasty and convenient snack — and they also give you a decent dose of insoluble fiber.

6. Almonds. Among nuts, almonds are highest in fiber, although other popular varieties such as pistachios and pecans are close behind. Walnuts have the added advantage of being a good source of polyunsaturated, plant-based omega-3 fatty acids.

7. Kiwi fruit. Contrary to popular belief, you don’t need to peel these fuzzy, brown fruits. But to avoid the skin, slice one in half and scoop out the inside with a spoon for an easy, fiber-rich, sweet snack.

8. Berries. Because these fruits are packed with tiny seeds, their fiber content is higher than most other fruits. Raspberries and blackberries provide the most, but strawberries and blueberries are also good sources.

9. Cauliflower. This cruciferous veggie not only provides fiber, but it can also serve as a substitute for white rice. Just shred or whirl in a food processor until it resembles rice, then sauté with a little olive oil until tender.

10. Soy. Eating soybeans and foods made from them, such as soymilk, tofu, and tempeh, was once touted as a powerful way to lower cholesterol. More recent analyses showed the effect is modest, at best. Still, protein-rich, soy-based foods are a far healthier choice than a hamburger or other red meat.

11. Salmon. Likewise, eating cold-water fish such as salmon twice a week can lower LDL by replacing meat and delivering healthy omega-3 fats. Other good fish options include chunk light canned tuna and tinned sardines.

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Depending on the type of fats and oils, they can either be implicated in the development of a disease or one that can prevent diseases that may be caused by another kind of fat.

For instance, fats and oils have a very significant role to play concerning the health of the arteries, the heart, and the brain. This is occasioned by their involvement in the formation of arteriosclerosis. As we already are aware, this is the deposition of plaques on the arteries that eventually lead to the blockage of the vessels. The blockage of the vessels results in coronary artery disease, heart attack, and stroke.

The type of fats implicated in the formation of arteriosclerotic plaques is saturated fats, trans fats, cholesterol, and triglycerides.

As stated earlier, cholesterol is not appreciably water-soluble and to be transported in the bloodstream, which is predominantly water-based, it has to be bound to lipoproteins. Two major kinds of lipoproteins that we are interested in are the Low-Density Lipoprotein (LDL) and the High-Density Lipoprotein (HDL). When cholesterol is bound to LDL, we have what is known as LDL-Cholesterol. HDL bound to cholesterol is known as HDL-cholesterol. The LDL when bound to cholesterol is referred to as ‘bad’ LDL-cholesterol and if it is bound to HDL, it is known as ‘good’ HDL-cholesterol. Cholesterol is never bad or good but this description has been given because of the direction of transport of cholesterol when it is bound to the lipoproteins. The LDL, which transports cholesterol from the liver to the cells, increases the risk of plaque formation as cholesterol accumulates in the blood vessels. On the other hand, the HDL transports cholesterol from the cells to the liver where it is excreted in the bile. What this means, is that, if there is more HDL-cholesterol in circulation, the risk of arteriosclerosis and heart disease will be significantly reduced. When LDL-cholesterol becomes higher, therefore, the risk of arteriosclerosis and heart attack increases.

In considering what kind of fats and oils one should be eating, the effect of the diet on HDL or LDL must never be overlooked. For example, trans fats increase LDL-cholesterol and decrease HDL-cholesterol. Polyunsaturated and monounsaturated fatty acids represented by omega 3 and 6; increase HDL-cholesterol, while decreasing LDL-cholesterol. Saturated fats increase both the ‘bad’ LDL-cholesterol and the ‘good’ HDL-cholesterol.

We also need to remember that the consistency of the fats and oils differentiate between the animal fats and plant fats. Animal fats, mainly saturated fats are solid at room temperature, while the plant fats, more often referred to, as oils are liquid at room temperature. Trans fats, which are solid at room temperature, are partially hydrogenated fat and have been described as the worst kind of fat a human being can consume. Trans fats increase LDL-cholesterol and decrease HDL-cholesterol. Examples of common trans fats are margarine and shortening. These along with oils that are used for deep-frying of things such as potatoes and chicken should be avoided.

Saturated fats tend to increase the level of cholesterol in the blood and for this reason, nutritionists advise that this kind of fats, if not avoided completely should be eaten less frequently. To be sure, I have reproduced the sources of saturated fats as a guide for us: Fatty portions of red meat, pork, chicken, and turkey eaten with the skin, butter, dairy products such as whole milk, cheese, cream, and fried and baked foods. Some prepared foods, for example, sausage, pizza, and desserts are also high in saturated fats. There are certain oils from plants like palm oil, palm kernel oil, and coconut oil that are saturated fats but do not contain cholesterol.

The best kind of fatty acids are monounsaturated and polyunsaturated fatty acids. They both increase HDL-cholesterol and decrease LDL-cholesterol. They also reduce the risk of arteriosclerosis, coronary artery disease, heart attack, and stroke. Examples of these are omega 3 and 6 and they can be found in such plants as almonds, hazelnuts, macadamia nuts, peanuts, pecans, cashew nuts, avocados, and olives.

Polyunsaturated fats are predominantly found in flaxseed, walnuts (roasted), pumpkin seeds, sesame seeds, and sunflower seed. They are also found in freshwater fatty fish such as salmon, tuna, herring, sardines, mackerel, and trout.

As I bring this article to a close, the recommendation is: Eat more of the unsaturated fatty acids – omega 3 and 6, less of saturated fats, and none of the trans fats.

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