Gary‘s Daily Health News - Vol. 7

Eating walnuts daily lowered bad cholesterol and may reduce cardiovascular disease risk

Hospital Clínic of Barcelona in Spain, Aug. 30,2021 

Eating about ½ cup of walnuts every day for two years modestly lowered levels of low-density lipoprotein (LDL) cholesterol, known as “bad cholesterol,” and reduced the number of total LDL particles and small LDL particles in healthy, older adults, according to new research published today in the American Heart Association’s flagship journal Circulation.

Walnuts are a rich source of omega-3 fatty acids (alpha-linolenic acid), which have been shown to have a beneficial effect on cardiovascular health.

“Prior studies have shown that nuts in general, and walnuts in particular, are associated with lower rates of heart disease and stroke. One of the reasons is that they lower LDL-cholesterol levels, and now we have another reason: they improve the quality of LDL particles,” said study co-author Emilio Ros, M.D., Ph.D., director of the Lipid Clinic at the Endocrinology and Nutrition Service of the Hospital Clínic of Barcelona in Spain. “LDL particles come in various sizes. Research has shown that small, dense LDL particles are more often associated with atherosclerosis, the plaque or fatty deposits that build up in the arteries. Our study goes beyond LDL cholesterol levels to get a complete picture of all of the lipoproteins and the impact of eating walnuts daily on their potential to improve cardiovascular risk.”

In a sub-study of the Walnuts and Healthy Aging study, a large, two-year randomized controlled trial examining whether walnuts contribute to healthy aging, researchers evaluated if regular walnut consumption, regardless of a person’s diet or where they live, has beneficial effects on lipoproteins.

This study was conducted from May 2012 to May 2016 and involved 708 participants between the ages of 63 and 79 (68% women) who were healthy, independent-living adults residing in Barcelona, Spain, and Loma Linda, California.

Participants were randomly divided into two groups: active intervention and control. Those allocated to the intervention group added about a half cup of walnuts to their usual daily diet, while participants in the control group abstained from eating any walnuts. After two years, participants’ cholesterol levels were tested, and the concentration and size of lipoproteins were analyzed by nuclear magnetic resonance spectroscopy. This advanced test enables physicians to more accurately identify lipoprotein features known to relate to the risk of cardiovascular disease.

The two-year study had a 90% retention rate (632 participants completed the study). Complete lipoprotein analyses were available in 628.

Among key findings of all study participants:

• At 2 years, participants in the walnut group had lower LDL cholesterol levels - by an average of 4.3 mg/dL, and total cholesterol was lowered by an average of 8.5 mg/dL.
• Daily consumption of walnuts reduced the number of total LDL particles by 4.3% and small LDL particles by 6.1%. These changes in LDL particle concentration and composition are associated with a lower risk of cardiovascular disease.
• Intermediate Density Lipoprotein (IDL) cholesterol also decreased. It is known that IDL cholesterol is a precursor to LDL and refers to a density between that of low-density and very-low-density lipoproteins. In the last decade, IDL cholesterol has emerged as a relevant lipid cardiovascular risk factor independent of LDL cholesterol.
• LDL cholesterol changes among the walnut group differed by sex; in men, LDL cholesterol fell by 7.9% and in women by 2.6%.

“While this is not a tremendous decrease in LDL cholesterol, it’s important to note that at the start of the study all our participants were quite healthy, free of major non-communicable diseases. However, as expected in an elderly population, close to 50% of participants were being treated for both high blood pressure and hypercholesterolemia. Thanks in part to statin treatment in 32%, the average cholesterol levels of all the people in our study were normal,” Ros said. “For individuals with high blood cholesterol levels, the LDL cholesterol reduction after a nut-enriched diet may be much greater.”

“Eating a handful of walnuts every day is a simple way to promote cardiovascular health. Many people are worried about unwanted weight gain when they include nuts in their diet,” Ros said. “Our study found that the healthy fats in walnuts did not cause participants to gain weight.”

The major limitation of this investigation is that both participants and researchers knew who was and was not eating walnuts. However, the study did involve two very different populations with distinct diets. “The outcomes were similar in both groups, so we can safely apply the results of this study to other populations,” Ros said. More research is also needed to clarify the different LDL results in men and women.

 

 

Research suggests potential for curcumin against demyelinating diseases

National Institute of Health (Italy), August 27, 2021

According to news reporting originating in Rome, Italy, research stated, “Curcumin is a compound found in the rhizome of Curcuma longa (turmeric) with a large repertoire of pharmacological properties, including anti-inflammatory and neuroprotective activities. The current study aims to assess the effects of this natural compound on oligodendrocyte progenitor (OP) differentiation, particularly in inflammatory conditions.”

The news reporters obtained a quote from the research from the National Institute of Health, “We found that curcumin can promote the differentiation of OPs and to counteract the maturation arrest of OPs induced by TNF-a by a mechanism involving PPAR-g (peroxisome proliferator activated receptor), a ligand-activated transcription factor with neuroprotective and anti-inflammatory capabilities. Furthermore, curcumin induces the phosphorylation of the protein kinase ERK1/2 known to regulate the transition from OPs to immature oligodendrocytes (OLs), by a mechanism only partially dependent on PPAR-g. Curcumin is also able to raise the levels of the co-factor PGC1-a and of the cytochrome c oxidase core protein COX1, even when OPs are exposed to TNF-a, through a PPAR-g-mediated mechanism, in line with the known ability of PPAR-g to promote mitochondrial integrity and functions, which are crucial for OL differentiation to occur.”

According to the news reporters, the research concluded: “Altogether, this study provides evidence for a further mechanism of action of curcumin besides its well-known anti-inflammatory properties and supports the suggested therapeutic potential of this nutraceutical in demyelinating diseases.”

 

 

The bitter truth of added sugar: What excessive fructose consumption can do to our body

New review explains how overconsumption of fructose, a common additive in sweetened foods and beverages, can contribute to diseases

Tianjin Medical University (China), August 30, 2021

In today’s fast-paced world, the dependence on the widely available “fast” foods and beverages has risen. These foods are typically low in fiber and essential nutrients, and often consist of high amounts of added sugar. This shift in dietary trends, accompanied by a sedentary lifestyle, has been attributed to the rise in various metabolic disorders like diabetes, fatty liver disease, and heart disease. The concerning thing about sugar is that the more you eat it, the more you crave it—leading to a vicious cycle of excessive sugar consumption and poor health.

So what exactly is this added sugar and why is it so bad for us? To understand this, let us first understand the basics. Refined sugar (or “sucrose”) is structurally composed of two simple forms of sugars called “glucose” and “fructose.” Although these simple sugars are structurally similar to each other, they are metabolized via different pathways in the body. And while excessive fructose intake (even within “normal” ranges, to some extent) has been shown to be harmful for us, the underlying mechanisms behind fructose metabolism and their potential role in metabolic disorders have not been fully understood so far.

Researchers from China, thus, sought to understand the fate of dietary fructose in the body and pathways regulating its metabolism, in a comprehensive review published in Chinese Medical Journal. Explaining the clinical implications of their study, Prof. Weiping J. Zhang, corresponding author of the study, says, “Our review provides a comprehensive update on the progress on molecular and cellular aspects of fructose metabolism and their role in the development of metabolic diseases. These findings can aid the development of new diagnostic, preventative, and therapeutic strategies for metabolic diseases.”

The researchers begin by explaining that most of the fructose that we ingest is absorbed by cells lining the intestine. Protein transporters called GLUT5 and GLUT2, expressed by intestinal cells, facilitate this absorption, with GLUT5 showing the highest affinity to fructose. Interestingly, these receptors are regulated in response to fructose levels, and thus, GLUT5 deficiency can result in fructose malabsorption and intestinal dysfunction. In fact, studies in mice have shown that deletion of GLUT5 can cause intestinal problems like gas and fluid accumulation. This is why, GLUT5 is a potential drug candidate for certain fructose-induced diseases.

Now when fructose enters circulation, its levels in the blood (albeit much lower than glucose) are kept at bay by the kidney and liver, both crucial metabolic hubs in our body. In these organs, fructose is redirected for glucose production, via a process called “gluconeogenesis.” However, this reaction requires the breakdown of a molecule called “ATP” (the main source of energy in cells). Thus, an excessive intake of fructose can lead to ATP depletion in cells, which activates another pathway involved in uric acid metabolism—leading to an accumulation of uric acid in the blood and joints and increasing the risk of developing “gout” (a condition causing severe joint pain). The researchers further explain that fructose consumption can also trigger an increase in cholesterol levels and abdominal fat, increasing the risk of heart disorders.

Next, the study talks about gene-level changes that regulate fructose metabolism. A protein called “ChREBP” is a crucial regulator of genes involved in the absorption, transport, and degradation of sugars. Animal studies in ChREBP-deficient mice now suggest that ChREBP is essential for fructose absorption and clearance. The molecular mechanisms regulating ChREBP activation in response to fructose stimulation, however, remain less understood. Prof. Zhang explains, “Obtaining a better understanding of the biochemical regulatory mechanism of ChREBP pathway can definitely provide new clues into the regulation of fructose metabolism and its metabolic effects. Future advances in this field will benefit our efforts to achieve better cardiometabolic health and inform clinical recommendations on the dietary intake of sugar.”

Overall, these findings shed light on how an increase in fructose consumption can lead to an imbalance in various metabolic pathways in our body and subsequently cause various diseases.

Indeed, what we eat plays a huge role in our overall health!

 

 

 

Olive oil compound may protect against AGE-induced toxicity

Università degli Studi della Campania (Italy), August 30, 2021

According to news originating from Naples, Italy, by NewsRx correspondents, research stated, “Hydroxytyrosol (HT), the major phenolic compound in olive oil, is attracting increasing interest for its beneficial properties including a notable antioxidant and anti-inflammatory power.”

Financial supporters for this research include Ministero dell’Istruzione, dell’Universita e della Ricerca.

The news correspondents obtained a quote from the research from Department of Precision Medicine: “In this study, using a combination of biophysical and cell biology techniques, we have tested the role of HT in the formation of advanced glycation end-products (AGEs). AGEs have a key role in clinical sciences as they have been associated to diabetes, neurodegenerative and cardiovascular diseases. In addition, as the incidence of Alzheimer’s disease (AD) is strongly increased in diabetic patients, AGE formation is supposed to be involved in the development of the pathological hallmarks of AD. Our data show that HT selectively inhibits protein glycation reaction in human insulin, and it is able to counteract the AGE-induced cytotoxicity in human neurotypical cells by acting on SIRT1 level and oxidative stress, as well as on inflammatory response.”

According to the news reporters, the research concluded: “This study identifies new beneficial properties for HT and suggests it might be a promising molecule in protecting against the AGE-induced toxicity, a key mechanism underlying the development and progression of neurodegenerative disorders.”

 

 

 

Breast cancer survivors increase the risk of dying prematurely when eating grilled and smoked meats

University of North Carolina, August 30, 2021

Now, disturbing study results show that female breast cancer survivors who ate more grilled, barbecued and smoked meats had a greater risk of dying, compared to those with lower intakes. Keep reading to discover how cooking meats at high temperatures can generate dangerous toxins – and the best way to protect your health.

The study, conducted at University of North Carolina Chapel Hill and published in the Journal of the National Cancer Institute, followed 1,508 women diagnosed with breast cancer for a median 17.6 years. During this time, 597 deaths occurred – 237 of which were associated with breast cancer.

Researchers found that having a higher intake of meats prior to the breast cancer diagnosis was associated with a 23 percent risk of dying from any cause. And, having higher amounts of grilled, barbecued and smoked meats after the diagnosis of breast cancer carried an increased mortality rate of 31 percent – a very substantial rise.

Other studies have mirrored the results of the research, and shown that the incidence of certain types of cancers increases among people who eat meat cooked at high temperatures.

In a University of Minnesota study, women who ate overcooked hamburgers increased their breast cancer risk by more than 50 percent compared to those who consumed their burgers rare or medium.

And an Iowa Women’s Health Study found that women who regularly ate well-done steak, hamburgers and bacon had a shocking 4.62-fold increase in their risk of developing breast cancer.

Experts say that eating foods cooked at high temperatures – through grilling, broiling, roasting, searing or frying – can expose the body to dangerous chemicals and DNA-altering mutagens known as glycotoxins, or “advanced glycation end products.”

These harmful compounds are released by the “browning” reaction – the darkening that gives grilled meat its charred appearance. The browning reaction produced by cooking at high temperatures causes the release of polycyclic aromatic hydrocarbons and heterocyclic amines, both of which are linked to cancers of the breast and prostate.

Advanced glycation end products, or AGEs, not only occur naturally in foods, but can be formed in the body through normal metabolism.

However, excessively high amounts in tissues and bloodstream can become pathogenic. AGEs cause tissue-damaging oxidative stress and produce chronic inflammation – factors that are at the root of degenerative chronic disease. They can also alter enzymes, hormones, antibodies and neurotransmitters – while damaging cell DNA and increasing susceptibility to cancer.

And, the acronym “AGE” is an apt one. Many experts believe that these glycotoxins can trigger weight gain and even premature aging.

Animal studies have shown that AGE-rich diets are associated with atherosclerosis and kidney diseases. In contrast, researchers found that reducing dietary AGEs in humans with diabetes reduced markers of inflammation and oxidative damage.

Avoiding exposure to highly cooked foods is a good place to start. Experts recommend using “moist heat” methods of cooking, such as poaching, steaming, boiling and stewing – along with using shorter cooking times and cooking at lower temperatures. (Of course, you still want to be sure that meats are fully cooked).

Interestingly, cooking with acidic ingredients – such as lemon or vinegar in marinades – can dramatically cut production of AGEs.

You can also adjust your food choices to generate fewer AGEs. Animal-based foods such as meats and poultry are naturally high in AGEs – and cooking triggers the formation of even more. For example, pan-fried beef contains a whopping 9,052 kilounits of AGEs per serving – and bacon rings in at 11,905 kilounits.

On the other hand, plant-based foods such as vegetables, whole grains, fruits and nuts have much lower levels of AGEs.  As a general rule, the more protein and fat a food contains, the more likely it is to be high in AGEs.

Studies have shown that certain supplements, including carnosine, benfotiamine and pyridoxal-5-phosphate, can function as anti-glycation agents. And indole-3-carbinol, an anti-cancer compound found in cruciferous vegetables, can sharply reduce damage from AGEs.

If you absolutely can’t resist indulging in an occasional sizzling steak, it would probably be wise to prepare it with an acidic marinade, and generous amounts of broccoli and Brussels sprouts on the side.

 

 

Cocoa flavanols may protect against diabetes: Study

Brigham Young University, August 31, 2021

Specific compounds within cocoa promote the release of insulin and may help protect against the onset of type-2 diabetes (T2D), reports a new study in Journal of Nutritional Biochemistry.

Adequate insulin production and protection of beta islet cells in the pancreas are both recognised to be important in the prevention of T2D.   

Monomeric cocoa catechins were found to stimulate insulin production in the pancreatic beta cells of rats. Additionally, these compounds, also known as flavanols, helped protect against death of these cells when exposed to high doses of fat, discovered the team led by researchers from Brigham Young University (BYU), Utah.

The catechins exerted their effect by increasing mitochondrial respiration in the cells, which in turn raises the production of adenosine triphosphate (ATP) – the molecule that transports energy within the cells.

"What happens is it's protecting the cells, it's increasing their ability to deal with oxidative stress," explained lead researcher, Professor Jeffery Tessem from BYU. "The epicatechin monomers are making the mitochondria in the beta cells stronger, which produces more ATP (a cell's energy source), which then results in more insulin being released."

The findings may have applications in the fight against the growing epidemic of T2D.   

"These results will help us get closer to using these compounds more effectively in foods or supplements to maintain normal blood glucose control and potentially even delay or prevent the onset of type-2 diabetes," said study co-author Professor Andrew Neilson, from Virginia Tech.

Small molecule effect

The researchers found that only the smaller molecules in cocoa extract – ‘monomeric’ catechins had the effect of increasing insulin production. The larger ‘oligomeric’ and ‘polymeric’ procyanidins and the whole cocoa extract actually slightly decreased insulin production.

Previous research has shown that the catechin monomer fraction of cocoa extract has the highest bioavailability when taken orally. Combined with the findings from this study that the monomeric flavanols are the most bioactive compounds, “suggests great potential for translation from in vitro cell culture to in vivo efficacy in animals and humans,” wrote the researchers.

Although the larger molecules’ (the oligomeric and polymeric procyanidins) influence on beta cell function is neutral or slightly negative, some animal studies have suggested these fractions of the cocoa extract may be metabolised by gut bacteria to bioavailable compounds.

Further studies are ongoing to investigate the impact of these larger cocoa flavanols in vivo.

Unfortunately, the beneficial effect on insulin production is likely to be obtained only from cocoa extract and not from eating chocolate bars, caution the researchers.

"You probably have to eat a lot of cocoa, and you probably don't want it to have a lot of sugar in it," said Tessem. "It's the compound in cocoa you're after."

As such, the next step will be to look at ways of extracting the monomeric catechins from cocoa, enhancing the quantity produced and then investigate its potential use as a treatment for diabetes patients, suggested the researchers.