Day: 04/11/2023

Enzalutamide, combined with standard treatment, shows promise in prostate cancer

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A new trial is exploring an androgen receptor blocker in treating prostate cancer. FG Trade/Getty Images

  • A second-generation androgen receptor blocker added to other prostate cancer treatments improves five-year survival rates for people with metastasized disease.
  • The blocker, enzalutamide, improved outcomes in a range of prostate cancers even where chemotherapy is ineffective.
  • Enzalutamide works by reducing the ability of prostate cancer cells to bind to testosterone, which promotes cancer growth.

Adding a second-generation androgen receptor inhibitor when treating metastasized prostate cancerTrusted Source can increase survival rates at five years, according to a new study. The study reports the findings of ENZAMET, international open-label trials that took place at 83 sites in Australia, Canada, Ireland, New Zealand, the U.K., and the U.S.A.

Significantly more patients who received enzalutamide in addition to standard treatment survived after five years than those who received standard treatment alone.

The study found that enzalutamide increased survival rates when added to the standard treatment of testosterone suppression plus docetaxelTrusted Source chemotherapy, as well as to testosterone suppression alone.

The four-year survival rate for patients receiving standard therapy is 57%, while the five-year survival rate for those who also received enzalutamide was 67%.

The study is published in THE LANCET OncologyTrusted Source.

Early prostate cancer

Prostate cancer is the second-most common cancer in men after skin cancer. According to the American Cancer SocietyTrusted Source, about 288,300 new cases of prostate cancer are diagnosed each year, and 34,700 men die of the disease annually.

Prostate cancer occurs when cells in the prostate gland, which is located beneath the bladder and in front of the rectum, become cancerous.

Most, though not all, prostate cancers are slow-growing, and the disease is not fatal more often than it is. The ACS estimates there are more than 3.1 million men living in the U.S. with diagnosed prostate cancer.

For men who are diagnosed with early-stage prostate cancer that has not metastasized — that is, it has not advanced beyond the prostate gland — there are several common therapeutic approaches.

The most common treatments for such cases are radical prostatectomy — in which the prostate is removed — and radiotherapy. There is also “watchful waiting,” with which the cancer is actively monitored without treatment unless the disease advances. All three have similarly high survival rates of about 97%.

An additional option is focal therapy, in which cancerous tissue on the prostate is destroyed using any of several techniques, including cryotherapy, ultrasound, laser treatment, and photodynamic therapy.

Metastasized prostate cancer

Prostate cancer cell division is commonly fueled by the hormone testosterone, the primary male sex hormone, and one of the two androgens the body produces. It is primarily produced by the testicles, and less so by the adrenal glands.

About 90% of prostate cancer is hormone-sensitive, according to urologist Dr. Mehran Movassaghi, who was not involved in the study. “All prostate cells use testosterone as their main fuel,” he said.

For men whose prostate cancer has spread to other organs or parts of the body, physicians attempt to cut off the cancerous cells’ supply of testosterone or reduce their ability to use it.

When a lab technician examines a biopsy of hormone-dependent prostate cancer tissue, androgen receptors are typically visible on the surface of cancerous cells.

Suppressing testosterone

The primary element of the standard treatment for patients with metastasized prostate cancer is testosterone suppression, which can be achieved in two ways.

With orchiectomy, a surgical procedure removes one or both testicles. There is also “medical castration,” in which LHRH agonistsTrusted Source prevent the secretion of the pituitary gland’s luteinizing hormone. Without this hormone, the testicles no longer produce testosterone, typically leading them to shrink, sometimes becoming so small they can no longer be felt.

In higher-income countries, surgical castration is no longer commonly used. However, Dr. Movassaghi noted that in lower-income countries, “That’s still ‘standard of care.’”

When cancer becomes hormone-insensitive

In many cases, “the cancer learns to utilize other types of fuel, and then it becomes hormone-insensitive,” explained Dr. Movassaghi.

“The cancer has essentially outsmarted its normal pathway that the prostate uses,” he said.

When this occurs, it becomes more difficult to control the disease and androgen-receptor blockers may be added to treatment, and in some cases, docetaxel.

How enzalutamide improves treatment outcomes

Enzalutamide is a second-generation androgen-receptor blocker. Urologist Dr. David Shusterman was also not involved in the study.

Dr. Shusterman explained that enzalutamide is a better drug than earlier blockers because “it is more potent, which means that it is more effective at blocking the activity of androgen receptors in the body.”

In addition, he said, “it can block androgen receptors in more areas of the body, which can help to slow down the spread of cancer cells.”

“It has fewer side effects than first-generation inhibitors, which can make it a more attractive option for patients,” he added.

The researchers found that enzalutamide was effective across different cancers, which are classified according to two characteristics:

  • The volume of metastases — With high-volume prostate cancer, four or more cancerous bone lesions exist along with one or more lesions somewhere in the body beyond the pelvis or spine, or in the body’s visceraTrusted Source. Low-volume prostate cancer involves fewer than four bone lesions, and may involve visceral lesions.
  • Timing of sites — Cancers are also identified as being synchronous or metachronous. Synchronous cancers develop at the same time wherever they appear. Metachronous cancers are of different ages, suggesting more prolonged development.

While docetaxel is more effective than testosterone suppression alone for most prostate cancers, it has little value with metachronous low-volume cancer. Enzalutamide, however, is effective in such cases.

“The results of this study are groundbreaking in that they suggest that enzalutamide can significantly improve survival rates for men with this type of cancer,” said Dr. Shusterman.

Dr. Movassaghi added that the study makes it easier to convince patients to try enzalutamide. It also makes it easier “for us to have insurance companies cover these newer and more expensive drugs because it solidifies the fact that they are actually extending the life expectancy of all these patients.”

In the end, concluded Dr. Shusterman, the study “emphasizes the importance of ongoing research and development in the treatment of prostate cancer. The results of this trial suggest that new treatments are on the horizon that can significantly improve outcomes for patients.”

Higher magnesium intake linked to lower dementia risk

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Food such as dark chocolate, spinach, and nuts are rich in magnesium.

  • Researchers investigated how magnesium intake influences dementia risk factors.
  • They found that a higher magnesium intake is linked to lower dementia risk.
  • Further research is needed to confirm the results.

In 2019, 57.4 million people had dementia globally. By 2050, this figure is expected to rise to 152.8 million.

As there is currently no cure for dementia, many researchers emphasize preventative strategiesTrusted Source such as diet. Some studies suggest that dietary magnesium is linked to better cognitive functionTrusted Source and may reduce dementia risk.

One studyTrusted Source that followed 1,000 middle-aged adults for 17 years found that those taking the highest levels of magnesium had a 37% lower risk of developing dementia compared to those who took the least amount.

Further research on the link between magnesium and cognitive status could inform preventative strategies for dementia.

Recently, researchers investigated how magnesium intake over time affects dementia risk. They found that higher magnesium intake is linked to better brain health—especially in women.

“Although more research is needed on this topic, the results of this study suggest that higher magnesium intake is associated with improved brain health and may potentially also be linked to preserved mental function and a reduced or delayed risk of developing dementia,” Dr. Kelly Johnson-Arbor, medical toxicologist, co-medical director, and interim executive director at the National Capital Poison Center, who was not involved in the study, told Medical News Today.

The study was published in the European Journal of Nutrition.

350 vs. 550 mg of magnesium daily

For the study, the researchers included healthcare data from 6,001 participants aged 40–73 years old from the UK Biobank.

Data included blood pressure measurements, a magnetic resonance imaging (MRI) scan, and dietary magnesium intake over a 24-hour period five times over 16 months.

Over 95% of participants consumed stable amounts of magnesium over the study period. Some, however, increased their intake over time, while others decreased their intake.

In the end, they found that higher dietary magnesium intake was linked to larger brain volumes and smaller white matter lesions (WML)—both of which are indicators of dementia—in MRI scans.

They also found that consuming over 550 mg of magnesium daily is linked to a roughly one-year younger brain age by 55 years old than consuming 350 mg per day, which is close to the average daily intake.

This, they noted, means that increasing magnesium intake by 41% could improve brain health, preserve cognitive ability, and lower dementia risk.

They further found that high dietary magnesium intake was more neuroprotective for women than men, and post-menopausal women compared to premenopausal women.

However, they noted that the decreasing magnesium consumption over time was linked to larger brain volumes in women.

Links between magnesium intake and blood pressure measures were mostly non-significant.

How magnesium lowers dementia risk 

“It’s known that magnesium is a neuroprotector as well as it having positive effects on blood pressure,” Dr. Howard Pratt, D.O., psychiatrist and Behavioral Health Medical Director at Community Health of South Florida, Inc., who was not involved in the study, told MNT.

“High blood pressure in and of itself is a known risk factor for dementia. Increasing dietary intake of magnesium can have positive effects on cardiovascular health with the study subsequently showing a decrease in white matter lesions in middle to early old age,” he added.

Dr. Johnson-Arbor noted that magnesium might help reduce inflammation.

“As we age, we are likely to develop chronic medical conditions, such as kidney disease and vitamin D deficiency, that cause magnesium deficiency. Because magnesium deficiency may lead to decreased cellular messaging and enhanced inflammation within the brain, some studies have suggested that magnesium may be involved in the development of dementia and other neurologic conditions.”
— Dr. Johnson-Arbor

Magnesium’s effects on women’s health

MNT spoke to Dr. Bruce Albala, professor of environmental & occupational health at the University of California, Irvine, Program in Public Health, who was also not involved in the study, to understand what might explain the increased effects of magnesium on post-menopausal women.

“The authors propose that the higher magnesium intake might have resulted in less chronic inflammation in these older women. These results should be viewed as preliminary at this time, especially for the smaller magnesium dietary subgroups,” he said.

“One of the interesting things about estrogen is that it is a vasodilator meaning that it can help lower blood pressure, and post-menopausal women having lower estrogen levels can in fact result in higher blood pressure. This is evidenced by the increase in cardiovascular risks for heart attack in women after menopause.”
— Dr. Howard Pratt

Dr. Johnson-Arbor further noted that the difference might be linked to health conditions that occur at different rates in men and women that may impact the clinical effects of magnesium. She said, however, that the authors did not study the impacts of other health conditions.

Study limitations 

Dr. Albala noted that the study has several limitations. As the researchers did not include a follow-up MRI scan, it remains to be seen whether magnesium is protective later in life as the participants’ average age was 55 years old.

He added that as over 95% of participants had stable magnesium intake over 16 months, they had very little data on how changing magnesium intake over time affects dementia risk.

He further said that magnesium consumption does not necessarily correlate with actual magnesium levels in the body nor how it impacts tissues such as the brain.

Dr. Pratt added that the study investigated risk factors as opposed to dementia diagnoses.

“The thing that limits this study is that a person can have several risk factors for dementia but may never develop it. There are also limitations in the lack of understanding of when and to what extent magnesium exerts its neuroprotective effects on the brain,” he noted.

“Although the study authors took into account factors such as cholesterol levels, history of tobacco use, history of diabetes, physical activity, and alcohol intake when they created their analysis, they did not collect information on other conditions—such as other cancer, kidney disease, or other neurologic conditions—that may have impacted the findings in this study,” Dr. Johnson-Arbor further explained.

Should I take magnesium to ward off dementia?

MNT spoke with Dr. Naomi Jean-Baptiste, a board-certified emergency medicine physician, who was not involved in the study, about the study’s implications. She warned against taking too much magnesium.

“Like all nutrients in the body, there is an ideal range and too much magnesium can be harmful to your body. High levels of magnesium can cause muscle weakness, fatigue, low blood pressure, breathlessness, and even death. So, you must be careful and discuss with your doctor before adding more magnesium to your diet.”
— Dr. Naomi Jean-Baptiste

MNT also spoke with Dr. Jason Krellman, neuropsychologist and assistant professor of neuropsychology at Columbia University Medical Center, who was also not involved in the study, about the findings.

“Further research using highly controlled, experimental conditions and a study design that tracks people’s neurocognitive health over time is needed to study the potential neurological and cognitive benefits of a magnesium-rich diet,” he said.

“However, the study’s promising findings highlight that there are several risk factors for dementia that individuals can identify and reduce through healthy lifestyle choices, including heart-healthy eating habits, aerobic exercise as tolerated, and doing cognitively and socially stimulating activities that you enjoy.”

Why some experts think obesity may increase autoimmune risk

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What link is there between obesity and autoimmunity?

  • Immune-mediated and autoimmune diseases are linked with the irregular activity of the immune system. Common examples of these diseases include psoriasis, rheumatoid arthritis, multiple sclerosis, and type 1 diabetes.
  • A​ recent perspective piece in the journal Science suggests that obesity may contribute to autoimmune disease risk due to overactive nutrient and energy-sensing pathways.
  • The author of the essay suggests that reducing caloric intake and using certain medications may help counteract the associated risk for autoimmune diseases from obesity.

The immune system’s role is to defend against what is dangerous to the body. However, it does not always work as it should, which can lead to health problems.

There is a great need for research to understand what triggers autoimmunity — where the body turns against itself or acts abnormally.

A​ recent perspective piece published in Science by Dr. Giuseppe Matarese, a professor of immunology at the University of Naples Federico II in Naples, Italy, discusses how obesity and overnutrition could influence the regulation of the immune system.

Autoimmune, immune-mediated diseases

Note: There is a difference between autoimmune conditions and immune-mediated conditions. The term “immune-mediated” is an umbrella term for disorders with abnormalities in immune system activity. Autoimmune diseases are a subcategory of immune-mediated diseases. Expert commenters and the perspective piece author have chosen to use the term “autoimmune disorders” as an umbrella term instead of “immune-mediated.”

Over 23.5 million peopleTrusted Source in the United States have some type of autoimmune disease. Autoimmune diseases occur when the body’s immune system attacks healthy body tissues.

The specific tissues affected will impact how the disease develops and doctors’ treatment approaches. For example, psoriasis is an autoimmune disease that affects the skin, while hemolytic anemia damages the body’s red blood cells. Inflammation is a common component of many autoimmune diseases.

It is not completely clear what causes autoimmune and immune-mediated diseases. Research is ongoing to understand modifiable and non-modifiable risk factors.

For example, someone’s genetics may play a role in developing an autoimmune disease, but so can certain lifestyle choices. One area of interest is how diet and weight may affect the risk for autoimmune and immune-mediated diseases.

Dr. Jason Balette, a bariatric surgeon with Memorial Hermann in Houston, TX, explained to Medical News Today:

“There appears to be a clear correlation with obesity and autoimmune diseases like MS. This association has been demonstrated through cell signal pathways between adipose cells (fat cells) and the immune system. Just as malnutrition has been shown to decrease immune function, overnutrition (obesity) has been demonstrated to increase immune function leading to autoimmune diseases. Clearly, there is much to learn about these relationships and cell signals to help guide us with treatment plans in the future.”

Obesity as a factor in autoimmune disease

The perspective paper in Science looked at how excessive caloric intake and obesity may influence the risk for abnormal immune responses by the body.

Dr. Matarese wrote about the possible underlying mechanisms of obesity and excessive caloric intake that may affect the body’s immune response.

H​e proposed that people who consume an obesogenic Western diet, that is, a diet that can lead to obesity, have changes in their metabolic workload. Put simply, they experience metabolic overload, which has many implications at the cellular level.

First, he proposed that adipose tissues promote increased leptin and cytokine levels. Leptin is a hormone that influences hunger and appetite. CytokinesTrusted Source influence the activity and production of immune cells.

H​e further notes that the circulation of certain nutrients from high-calorie intake in obese individuals is also at work.

H​e proposed that these three factors combined lead to increased inflammatory response and abnormalities in the actions and cells of the immune system. These results then lead to an increased risk for autoimmune disorders.

D​r. Matarese explained some of the critical points of his paper to MNT:

“This perspective summarizes why today we observe a raising in frequency of autoimmune diseases in more affluent countries where there is a strong excess of calorie intake. Calories in excess induce activation of immune cells, thus leading to an increased chance to loose immunological self-tolerance. Generally, the amount of calories and the quality of foods, typically of western diets rich in lipids and carbs, induce inflammation by activating innate and adaptive immune cells and their production of inflammatory mediators, increasing the chance of developing autoinflammation.”

Continuing research and interventions

Based on the ideas he presents in the piece, Dr. Matarese suggests that behavioral interventions may help control the body’s autoimmune response. This could involve intermittent fasting and calorie restriction. It could also include using medications that mimic fasting and reduce the body’s inflammatory response.

Dr. Matarese also discussed that researchers need to go further in investigating different areas. “[We need to] understand specifically if specific diet regimens, not only the amount of calories, predispose to specific diseases more than others,” he told MNT.

Researchers should “also assess whether calorie restriction (CR) can be an effective additional treatment to improve autoimmunity together with specific drug treatments — i.e. there are ongoing trials associating calorie restriction to treat multiple sclerosis together with drugs such as dimethyl fumarate,” he added.

Commenting on the paper, Dr. Balette noted that it points to the importance of maintaining a healthy body weight and what further research could include. He elaborated to MNT:

“The connection between obesity and autoimmune diseases as well as other medical comorbidities related to obesity demonstrates the importance of the need for both surgical and non-surgical weight loss. The further research areas I would like to see would be the continued investigation of the cell signals like leptin, ghrelin and how they change in the post-operative bariatric surgical patient. In addition, further investigation with immunosuppressive and anti-inflammatory drugs and how they function in the obese patient.”

Ibuprofen Kills Thousands Each Year, so What Is the Alternative?

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(Shutterstock*)

Back in 2013, one Reuters article opened with the following stunning sentence: “Long-term high-dose use of painkillers such as ibuprofen or diclofenac is ‘equally hazardous’ in terms of heart attack risk as use of the drug Vioxx, which was withdrawn due to its potential dangers, researchers said.”

The 2004 Vioxx recall, as you may remember, was spurred by the nearly 30,000 excess cases of heart attacks and sudden cardiac deaths caused by the drug between 1999 and 2003. Despite the fact that scientific research had accumulated as early as 2000 linking Vioxx to increased heart attacks and strokes, the drug’s manufacturer, Merck, and the U.S. Food and Drug Administration remained silent as the death toll steadily increased. The Reuters report focused on research published in The Lancet indicating the risk of heart attack increases as much as a third and the risk of heart failure doubles among heavier users of non-steroidal anti-inflammatory drugs (NSAIDs).

Pain and unhealthy levels of inflammation are fast becoming default bodily states in the industrialized world. While, in most cases, we can adjust the underlying pro-inflammatory conditions by altering our diet, reducing stress, and avoiding environmental chemical exposures, these approaches take time, discipline, and energy. Sometimes we just want the pain to stop now. In those often compulsive moments, we find ourselves popping an over-the-counter pill to kill the pain.

The problem with this approach is that, if we do it often enough, the side effects accumulate and we put our lives at risk.

Ibuprofen really is a perfect example of this. As mentioned above, this petrochemical derivative has been linked to a significantly increased risk of heart attack and increased cardiac and all-cause mortality risk (when combined with aspirin). Among the more than two dozen serious adverse health effects, people taking these drugs may suffer:

  • Anemia
  • DNA Damage
  • Hearing Loss
  • Hypertension
  • Influenza Mortality
  • Miscarriage

Ibuprofen is, in fact, not unique in elevating cardiovascular disease risk and/or mortality. The entire category of NSAIDs appears to have this under-recognized dark side; cardiovascular disease and cardiac mortality score highest on the list of more than 100 unintended adverse health effects associated with their use.

So what does one do? Pain is pain. Whether it happens to you or you witness it in another (which can be worse), finding relief is a top priority.

Research on Natural Painkillers

Here’s some evidence-based research on alternatives to ibuprofen, sourced from the National Library of Medicine.

Ginger: A 2009 study found that ginger capsules (250 milligrams, four times daily) were as effective as the drugs mefenamic acid and ibuprofen for relieving pain associated with women’s menstrual cycle (primary dysmenorrhea).

Topical Arnica: A 2007 human study found that topical treatment with arnica was as effective as ibuprofen for hand osteoarthritis but with a lower incidence of side effects.

Astaxanthin, Ginkgo biloba, and Vitamin C Combined: A 2011 animal study found this combination to be equal to or better than ibuprofen for reducing asthma-associated respiratory inflammation.

Chinese Skullcap (Baicalin): A 2003 animal study found that a compound in Chinese skullcap known as baicalin was equal in effect to ibuprofen in reducing pain.

Omega-3 Fatty Acids: A 2006 human study found that omega-3 fatty acids (between 1200–2400 mg daily) were as effective as ibuprofen in reducing arthritis pain but with the added benefit of having fewer side effects.

Panax Ginseng: A 2008 animal study found that panax ginseng had analgesic and anti-inflammatory activity similar to ibuprofen, indicating its possible anti-rheumatoid arthritis properties.

St. John’s Wort: A 2004 animal study found that St. John’s wort was twice as effective as ibuprofen as a pain-killer.

Anthocyanins from Sweet Cherries and Raspberries: A 2001 cell study found that anthocyanins extracted from raspberries and sweet cherries were as effective as ibuprofen and naproxen at suppressing the inflammation-associated enzyme known as cyclooxygenase-1 and -2.

Holy Basil: A 2000 study found that holy basil contains compounds with anti-inflammatory activity comparable to ibuprofen, naproxen, and aspirin.

Olive Oil (oleocanthal): a compound found within olive oil known as oleocanthal has been shown to have anti-inflammatory properties similar to ibuprofen.

There are, of course, hundreds of additional substances that have been studied for their pain-killing and/or anti-inflammatory effects, and there are also aromatherapeutic approaches that don’t require the ingestion of anything at all.

But even here, with such seemingly gentle approaches, there’s danger.

When we think of taking an alternative pain-killer to ibuprofen, we’re still thinking within the palliative, allopathic medical model: suppress the symptom, and go on about our business.

It would behoove us to look deeper into what’s causing our pain. And when possible, remove the cause(s).

That often requires lifestyle changes, such as a dramatic dietary shift away from pro-inflammatory foods, many of which most Westerners still consider absolutely delightful.

23 Cancer Stem Cell Killing Foods Smarter Than Chemo and Radiation

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Peppermint is one of about 25 varieties of mint. (Oxana Denezhkina)

Peppermint is one of about 25 varieties of mint.

An important scientific review identifies 23 of the top foods and herbs which kill the cancer stem cells at the root cause of cancer malignancy

There are thousands of natural compounds that have been studied with demonstrable anti-cancer activity, but only a small subset of these have been proven to target and kill the cancer stem cells which lie at the root of cancer malignancy. Turmeric, for instance, we have featured a number of times for this “smart kill” property of targeting just the heart of cancerous tumors. More recently, ginger has been found in pre-clinical research to contain a compound up to 10,000 times more effective than the chemotherapy drug Taxol at killing breast cancer stem cells. Even common food like blueberry have special cancer killing properties, as discussed in a previous article: Research: Radiotherapy Causes Cancer, Blueberry Kills It.

A powerful study published in the journal Anticancer Research titled, “Natural Products That Target Cancer Stem Cells,” has made our job much easier of identifying this special category of cancer killers by reviewing the extant literature on the topic and listing the top 25 substances in this category. They are listed here below, along with some of their commonly recognizable dietary sources:

  1. Epigallocatechin-3-gallate (EGCG) – Green Tea
  2. 6-Gingerol – Ginger
  3. β-Carotene – Carrot, Leafy Greens
  4. Baicalein – Chinese Skullcap
  5. Curcumin – Turmeric
  6. Delphinidin – Blueberry, raspberrry
  7. Flavonoids (Genistein) – Soy, red clover, coffee
  8. Guggulsterone – Commiphora (myrrh tree)
  9. Isothiocyanates – Cruciferous vegetables
  10. Linalool – Mint
  11. Lycopene – Grapefruit, tomato
  12. Parthenolide – Feverfew
  13. Perylill alcohol – Mint, cherry, lavender
  14. Piperine – Black pepper
  15. Platycodon saponin – Platycodon grandiflorum
  16. Psoralidin – Psoralea corylilyfolia
  17. Quercetin – Capers, onion
  18. Resveratrol – Grapes, plums, berries
  19. Salinomycin – Streptomyces albus
  20. Silibinin – Milk Thistle
  21. Ursolic acid – Thyme, basil, oregano
  22. Vitamin D3 – Fish, egg yolk, beef, cod liver oil
  23. Withaferin A – Withania somnifera (ashwaganda)

Why Are These Substances so Important?

The primary reason why conventional chemotherapy and radiotherapy have failed to produce any significant improvements in cancer survival rates is because cancer stem cells are resistant to these interventions. In fact, chemotherapy and especially radiation are both capable of increasing the number and virulence of these cells in a tumor, while at the same time having the well known side effect of further damaging the patient’s immune system.

While the cancer industry is still very much resistant to incorporating the implications of these findings into their standard of care (which is highly unethical), there are an increasing number of health practitioners that will not turn their back on the truth and are very much interested in alternative ways to prevent and treat cancer using food and/or plant-based approaches.

The new study addresses the relevance of cancer stem cells as follows:

The cancer stem cell model suggests that tumor initiation is governed by a small subset of distinct cells with stem-like character termed cancer stem cells (CSCs). CSCs possess properties of self-renewal and intrinsic survival mechanisms that contribute to resistance of tumors to most chemotherapeutic drugs. The failure to eradicate CSCs during the course of therapy is postulated to be the driving force for tumor recurrence and metastasis. Recent studies have focused on understanding the unique phenotypic properties of CSCs from various tumor types, as well as the signaling pathways that underlie self-renewal and drug resistance.

At present, the cancer industry has failed to produce a single drug that targets the cancer stem cell population of cells within a tumor, as confirmed by the study:

If indeed the CSC response is a vital criterion for cancer treatment evaluation, there are still no drugs in clinical use that specifically target CSCs.

The ability to selectively target cancer cells, and cancer stem cells in particular, while leaving intact the non-tumor cells in tissue is extremely important. We have created a section on our database that indexes research on these substances and now includes sixty seven of them here.

SGLT2 inhibitor therapy reduces sudden cardiac death risk in heart failure

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Key takeaways:

  • Patients with heart failure who received an SGLT2 inhibitor were less likely to experience sudden cardiac death vs. placebo.
  • There was no reduction in arrhythmic events observed with SGLT2 inhibitor use.

SGLT2 inhibitor therapy in patients with heart failure is associated with a significantly lower incidence of sudden cardiac death vs. placebo, with the benefit persisting independent of other guideline-directed medical therapies.

“The decreased incidence of sudden cardiac death in patients with HF receiving SGLT2 inhibitor therapy is directly concordant with studies demonstrating that SGLT2 inhibitor therapy has a profound impact on CV death and heart failure hospitalizations in patients with heart failure regardless of ejection fraction,” Connor Oates, MD, a cardiovascular disease fellow with MedStar Heart and Vascular Institute and Georgetown University-Washington Hospital Center, and colleagues wrote in Clinical Cardiology. “Patients with heart failure, whether characterized as HF with reduced ejection fraction or HF with preserved EF, develop fibrosis, myocardial hypertrophy, electrical and metabolic dysregulation that can predispose to atrial and ventricular tachyarrhythmias, bradyarrhythmias and other electromechanical disorders. These different mechanisms can independently lead to sudden cardiac death in patients with HF and can be directly impacted by SGLT2 inhibitor therapy.”

Heart failure_Adobe Stock_192824687
Patients with heart failure who received an SGLT2 inhibitor were less likely to experience sudden cardiac death vs. placebo.

Oates and colleagues analyzed data from seven trials published before Aug. 28, 2022, that included participants with HF that compared the use of an SGLT2 inhibitor (n = 10,796) vs. placebo (n = 10,796) and reported on outcomes including sudden cardiac death, ventricular arrhythmias and atrial arrhythmias.

SGLT2 inhibitor therapy was associated with a significant reduction in risk for sudden cardiac death (RR = 0.68; 95% CI, 0.48-0.95; P = .03; I2 = 0%). Absent dedicated rhythm monitoring, there were no significant differences in the incidence of sustained ventricular arrhythmias not associated with sudden cardiac death (RR = 1.03; 95% CI, 0.83-1.29; P = .77; I2 = 0%) or atrial arrhythmias (RR = 0.91; 95% CI, 0.77-1.09; P = .31; I2 = 29%) between patients who received an SGLT2 inhibitor or placebo.

“Our analysis did not demonstrate a reduction in the incidence of arrhythmic events in patients receiving SGLT2 inhibitor therapy,” the researchers wrote. “This finding, although consistent with a post-hoc analysis of DAPA-HF, is limited by the design of trials included, specifically a lack of dedicated rhythm monitoring.”

The researchers wrote that it is essential for future randomized trials of HF therapies to include dedicated rhythm monitoring to improve the characterization of sudden death.

AI identifies reasons for statin nonuse in patients with diabetes at a single center

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Key takeaways:

  • An AI model identified reasons for statin nonuse among patients with diabetes.
  • The most common reasons included statin hesitancy, guideline-discordant practice and clinical inertia.

A deep learning model utilized unstructured electronic health record data to identify specific patient-, physician- and system-level reasons for statin nonuse among patients with diabetes, researchers reported.

Reasons for statin nonuse varied across age, race/ethnicity, insurance and diabetes type, according to the study published in the Journal of the American Heart Association.

Statins_AdobeStock
An AI model identified reasons for statin nonuse among patients with diabetes.
Image: Adobe Stock

“Our data showed gaps and disparities in real-world statin use in individuals with diabetes, and an AI approach can be helpful in assessing complex, unstructured clinical notes to shed light on understanding the reasons behind statin nonuse in a health system,” Ashish Sarraju, MD, former fellow in cardiovascular medicine at Stanford University and current staff cardiologist at Cleveland Clinic, told Healio. “The statin nonuse seen in this study — and a prior study we did with patient with established atherosclerotic CVD — was consistent with what has been described in the literature, so we were not surprised. We knew from prior work that our AI approach performed well with assessing clinical notes, but we were still encouraged by how well it could identify complex reasons for statin nonuse.”

Ashish Sarraju

To test their hypothesis, Sarraju and colleagues developed a deep learning NLP algorithm using Clinical Bidirectional Encoder Representations from Transformers (BERT) to identify statin nonuse and actionable reasons for nonuse among 33,461 patients with diabetes at Stanford Health Care Alliance (mean age, 59 years; 49% women; 36% white).

Accuracy of Clinical BERT

The algorithm’s performance was evaluated against expert clinician review and compared with other NLP approaches.

Sarraju and colleagues observed Clinical BERT successfully identify statin nonuse with an area under receiver operating characteristic curve of 0.99 and patient, clinician and system reasons for statin nonuse with an AUC of 0.9.

The researchers reported that Clinical BERT demonstrated good concordance with expert clinician review and outperformed other NLP approaches.

Overall, 47% of the cohort had no statin prescriptions and 16% were using a statin despite no documented statin prescriptions.

Researchers reported that statin hesitancy (19%), guideline-discordant practice (19%) and clinical inertia (18%) were more common compared with side effects and/or contraindications (12%) as the reason for statin nonuse.

Specific reasons for statin nonuse

Reasons for nonuse varied by age, race/ethnicity, insurance and diabetes type, according to the study.

Patients older than 75 years were more likely to experience statin-associated side effects and/or contraindications than statin hesitancy, clinical inertia or discordant practice compared with younger patients (P < .05).

Hispanic individuals were most likely to experience guideline-discordant practice compared with most other reasons for statin nonuse (P < .05), whereas Black patients were most likely to experience clinical inertia as their reason (P < .05), according to the study.

Patients with Medicaid insurance were more likely to experience guideline-discordant practice compared with the other reasons for nonuse (P < .05).

Moreover, patients with type 1 diabetes were more likely to experience guideline-discordant practice compared with the other reasons for statin nonuse (P < .05), according to the study.

Fatima Rodriguez

“Like many health systems, Stanford is developing dashboards and decision support tools to ensure that patients are receiving guideline-directed statin therapy,” Fatima Rodriguez, MD, MPH, FACC, FAHA, associate professor of cardiovascular medicine and section chief of preventive cardiology at Stanford University School of Medicine, told Healio. “Still, gaps in use of evidence-based therapies are pervasive. Our study highlights that augmenting structured data in clinical notes can help understand some of the reasons behind these gaps and help develop health-system-level interventions to address them.”

Top Concentration Killers

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Culprit: Social Media

Culprit: Social Media

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Whether you’re living with ADHD or just have trouble focusing from time to time, today’s world is full of concentration killers. Psychologist Lucy Jo Palladino, PhD offers a few tips to manage distractions, starting with social media. It’s easy to connect with friends — and disconnect from work — many times an hour. Every status update zaps your train of thought, forcing you to backtrack when you resume work.

Social Media Fix

Social Media Fix

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Avoid logging in to social media sites while you’re working. If you feel compelled to check in every now and then, do it during breaks, when the steady stream of posts won’t interrupt your concentration. If you can’t resist logging in more frequently, take your laptop someplace where you won’t have Internet access for a few hours.

Culprit: Email Overload

Culprit: Email Overload

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There’s something about an email — it shoots into your inbox and itches to be answered immediately. Although many emails are work-related, they still count as distractions from your current project. You won’t make much progress if you constantly stop what you’re doing to reply to every message.

Email Overload Fix

Email Overload Fix

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Instead of checking email continuously, set aside specific times for that purpose. During the rest of the day, you can actually shut down your email program. This allows you to carve out blocks of time when you can work uninterrupted.

Culprit: Your Cell Phone

Culprit: Your Cell Phone

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Perhaps even more disruptive than the ping of an email is the ringtone on your cell phone. It’s a sound few of us can ignore. But taking a call not only costs you the time you spend talking — it can also cut off your momentum on the task at hand.

Cell Phone Fix

Cell Phone Fix

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Put caller ID to good use. If you suspect the call is not urgent, let it go to voicemail. If you’re working on a particularly intense project, consider silencing your phone so you’re not tempted to answer. Choose specific times to check voicemail. Listening to all your messages at once can be less disruptive than taking every call as it comes in.

Culprit: Multitasking

Culprit: Multitasking

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If you’ve mastered the art of multitasking, you probably feel you’re getting more done in less time. Think again, experts say. Research suggests you lose time whenever you shift your attention from one task to another. The end result is that doing three projects simultaneously usually takes longer than doing them one after the other.

Multitasking Fix

Multitasking Fix

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Whenever possible, devote your attention to one project at a time, particularly if you’re working on an intense or high-priority task. Save your multitasking skills for chores that are not urgent or demanding — it probably won’t hurt to tidy up your desk while talking on the phone.

Culprit: Boredom

Culprit: Boredom

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Some of the tasks we have to do each day are more interesting than others. The boring ones may burn through your attention span in minutes, making you extremely vulnerable to distractions. Your phone, the Internet, even the prospect of dusting your workspace can seem tempting if you’re bored.

Boredom Fix

Boredom Fix

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Make a deal with yourself: If you stay on task for a certain period of time, you earn a 10-minute break. Reward yourself with coffee, a favorite snack, or a walk outside. Boring tasks are easier to accomplish when you have something to look forward to. This is also one case where multitasking may work well. Listening to the radio while filing receipts could help you stay put long enough to finish the job.

Culprit: Nagging Thoughts

Culprit: Nagging Thoughts

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It’s hard to focus on the work in front of you if you’re worrying about errands you need to run or housework to be done. Or perhaps you’re hung up on a conversation you had yesterday, and you keep replaying it in your mind. Nagging thoughts of any sort can be a powerful distraction.

Nagging Thoughts Fix

Nagging Thoughts Fix

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One way to keep nagging thoughts from buzzing around in your brain is to write them down. Make a list of errands, housework, or other tasks you plan to complete later. Vent frustrations over an unpleasant confrontation in your journal. Once these thoughts are on paper, you may be able to let them go for a while.

Culprit: Stress

Culprit: Stress

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When you feel like you have too much on your plate, it can be hard to focus on individual tasks. To make matters worse, stress takes a noticeable toll on the body. You may develop tight shoulders, headaches, or a racing heart, all of which can chip away at your ability to concentrate.

Stress Fix

Stress Fix

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Learn stress reduction techniques, such as meditation. This can help you rein in stressful thoughts, so they don’t demand so much of your attention. In one study, researchers found that people who took an eight-week meditation course improved their ability to focus. If you can’t find a meditation class locally, look for one online.

Culprit: Fatigue

Culprit: Fatigue

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Fatigue can make it tough to concentrate, even when you have few distractions. Studies suggest too little sleep can sap your attention span and short-term memory. 

Fatigue Fix

Fatigue Fix

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Most adults need 7-9 hours of sleep per night. Instead of burning the midnight oil, make sleep a priority. This will help you get more done during your waking hours. Also, pay attention to which times of day you feel most alert. Then you’ll know when to schedule your most intense tasks.

Culprit: Hunger

Culprit: Hunger

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The brain can’t focus without fuel, so skipping meals — especially breakfast —  is a top concentration killer. Research indicates short-term memory and attention suffer when you rise and shine but do not dine.

Hunger Fix

Hunger Fix

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Keep hunger at bay and give your brain a steady source of fuel with these habits:

  • Always eat breakfast.
  • Eat high-protein snacks (cheese, nuts)
  • Skip simple carbs (sweets, white pasta)
  • Choose complex carbs (whole grains)
Culprit: Depression

Culprit: Depression

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Most people tend to think of sadness as the hallmark of depression. But the National Institute of Mental Health says difficulty concentrating is one of the most common symptoms. If you’re having trouble focusing, and you also feel empty, hopeless, or indifferent, you may be experiencing depression.

Depression Fix

Depression Fix

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If you think you might be depressed, the first step is to talk with a doctor or counselor. Depression is highly treatable. Many studies have shown the effectiveness of antidepressant medications and certain types of talk therapy. 

Culprit: Medication

Culprit: Medication

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Unfortunately, some of the medications used to treat depression can interfere with concentration. The same is true of many other drugs. Talk to your doctor or pharmacist to check if a medication or supplement you are taking may be affecting your concentration.

Medication Fix

Medication Fix

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If you suspect your meds are clouding your concentration, don’t assume there are no other options. Talk to your doctor about adjusting your dosage or switching to a different class of medication. Do not stop taking your medicine unless your doctor tells you to.

Culprit: ADHD

Culprit: ADHD

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Attention deficit hyperactivity disorder (ADHD) is not just a problem for children. More than half of kids with ADHD continue to experience symptoms as adults. The classic signs are a short attention span and trouble focusing on tasks.

ADHD Fix

ADHD Fix

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If you have consistent trouble focusing, and you had attention problems as a child, ask a doctor or counselor about ADHD. There are ways to manage the condition, including behavioral therapy and medications.

A rat study offers clues about how ketamine can lead to psychosis

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  • Researchers investigated whether ketamine may induce changes in the brain that are similar to psychosis.
  • They found that ketamine increases background noise, which may interfere with how the brain processes sensory signals.
  • The researchers conducted their study on rats, meaning that further research is needed to see how the findings may apply to humans.

Schizophrenia is characterized by changes in how a person perceives reality, including experiencing persistent delusions, hallucinations, and disorganized thinking. The condition affects around 24 millionTrusted Source people globally.

The exact cause of schizophrenia remains unknown. However, studies suggest that the condition may arise from environmental, psychological, and genetic factors.

A drug known as ketamine induces a mental state similar to psychosis in healthy individuals by inhibiting NMDA receptorsTrusted Source in the brain. This creates an imbalance of excitatory and inhibitory signals in the central nervous system, which affects sensory perception.

Experts believe that similar changes in NMDA receptors could be linked to perception changes in schizophrenia. How this may be the case, however, has remained unknown.

Ketamine and psychosis

Recently, researchers examined how ketamine affects sensory perception in the brains of rats.

They found that ketamine increased “background noise” in the brain, making sensory signals less defined or pronounced. This, they noted, may explain the distorted perception of reality among people with schizophrenia or psychosis.

Their findings appeared in the European Journal of NeuroscienceTrusted Source.

Dr. Sam Zand, a psychiatrist based in Las Vegas, not involved in the study, commented on these findings, telling Medical News Today that they “suggest that dysfunction in NMDA receptors may play a role in the development of psychosis.”

“The study provides new insights into the mechanism by which ketamine may induce psychotic symptoms. The findings may help to inform the development of new treatments for psychosis that target NMDA receptors or brain noise,” he added.

The study design

For the study, the researchers looked at the effects of ketamine on sensory perception in seven male lab rats. To do so, they first implanted rats with electrodes to record electrical activity in their brains.

They then simulated their whiskers and recorded the brain’s responses before and after ketamine.

More specifically, the researchers monitored how ketamine affects beta and gamma oscillations in a neural network that transmits signals from sensory organs to the brain.

Beta oscillations are brainwaves that range from 17–29 Herz (Hz), while gamma waves range from 30–80 Hz. The frequencies are crucial for processing sensory information.

In the end, the researchers found that ketamine increased power in both beta and gamma oscillations even before they stimulated the rats’ whiskers.

They also found, however, that post-stimulus and after ketamine administration, the amplitude of the rats’ beta and gamma oscillations decreased, which is linked to impaired perception.

They further noted that ketamine increased noise in gamma frequencies, which is also linked to an impaired ability to process sensory signals.

The researchers suggested that their findings mean that the distorted reality experienced in psychosis and schizophrenia may be triggered by more background noise, which in itself may be caused by malfunctioning NMDA receptors causing an imbalance of inhibition and excitation in the brain.

“The discovered alterations in thalamic and cortical electrical activity associated with ketamine-induced sensory information processing disorders could serve as biomarkers for testing antipsychotic drugs or predicting the course of disease in patients with psychotic spectrum disorders,” says Dr. Sofya Kulikova, senior research fellow at the HSE University in Perm, Russia, one of the study authors.

Research limitations 

MNT spoke with Dr. Howard Pratt, psychiatrist and behavioral health medical director at Community Health of South Florida, not involved in the study, about its limitations. He emphasized that:

“The limitations of these findings are really that while we have clear correlation, we don’t yet have causation. Conditions like psychosis have numerous causes, which could be, for example, elevations in dopamine, which is the target of treatment with people carrying a diagnosis of schizophrenia. I look forward to seeing what happens when the research goes beyond animal studies.”

We also spoke with Dr. James Giordano, Pellegrino Center professor of neurology and biochemistry at Georgetown University Medical Center, not involved in the study, about the study’s limitations.

“A major limitation of the study is that it only investigated ketamine-induced effects, and thus, while useful and viable for gaining insights to ketamine’s activity in a rat model, may not provide direct translation to understand non–drug–induced dissociative, and psychotic states in humans,” he cautioned.

“It may be, for example, that the effects produced by ketamine in humans, while certainly being dissociative, and having certain characteristics of psychosis, are not completely representative or identical to the neurological mechanisms involved in other types of psychosis and schizophreniform disorders,” Dr. Giordano further noted.

Potential clinical implications 

When asked about the study’s implications, Dr. Giordano explained that “[t]hese findings are useful in that demonstration of ketamine’s actions at defined brain networks may enable better understanding — and improved clinical applications — of its effects in humans.”

“Additionally, by illustrating the roles of these brain nodes and networks involved in mediating dissociative states, we may develop improved insights — and possible treatments for — certain types of drug-induced psychoses, and perhaps other psychotic conditions, such as forms of schizophrenia, as well,” he concluded.

Does Coffee Cause Inflammation?

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Waking up with a cup of coffee may be your tried and true morning ritual. But do you feel your best after caffeinating? Inflammation, especially over time, has been a hot topic for those looking into their healthy eating and living practices, and it may impact the way you enjoy your favorite beverage. 

To understand if you’re experiencing inflammation, here’s a little background on inflammation, including the different types. “Inflammation is the body’s immune system’s response to an irritant, where it starts to recognize and remove harmful components and starts the healing process,” explain Lyssie Lakatos, RDN and Tammy Lakatos Shames, RDN, also known as The Nutrition Twins. “Acute inflammation is a response to sudden damage in the body, like a sprained ankle, where the body sends inflammatory compounds to the injured area to protect it. Chronic inflammation is when your body continues to send inflammatory compounds even though the body is no longer in danger, and it starts to damage the body’s tissues and cells.” Chronic inflammation, or long-term inflammation, is linked with chronic disease. Additionally, chronic inflammation makes it harder to lose weight and easier to gain weight, which is why it’s a concern for many in the health and nutrition community. 

does-coffee-cause-inflammation-GettyImages-18541100

Luckily, sipping coffee may actually help acute or chronic inflammation, not cause it to flare up. “Coffee actually seems to reduce inflammation [according to a 2019 scientific review] and not cause it,” say The Nutrition Twins. “Coffee’s unique mixture of compounds and antioxidants, like chlorogenic acid, caffeine, cafestol, kahweol, and trigonelline, appear to play a part in reducing inflammation.

“And beyond reducing inflammation, drinking coffee can also help reduce risk of diseases in which inflammation plays a role in their progression, like heart disease, diabetes, and cancer,” The Nutrition Twins say. However, this may not be true for all people. “Keep in mind that some people are genetically inclined to be sensitive to caffeine, and for these people, coffee may create inflammation due to its caffeine content,” the pair adds.

 Drinking your coffee black, both hot and iced, can be anti-inflammatory. However, once you add sweeteners or dairy products—sugar, syrup, cream, or a whipped topping—you’re introducing pro-inflammatory components into your coffee, which trigger pro-inflammatory cytokines. “Additives like sugar cause low-grade chronic inflammation that is linked with autoimmune disease and other chronic diseases,” The Nutrition Twins state, citing a 2022 study that appeared in the medical journal, Frontiers in Immunology.

If you have a sweet tooth, the duo suggests flavoring your coffee with a sprinkle of cinnamon for natural sweetness, which will also increase the antioxidants in your cup. Adding a splash of unsweetened almond milk or another nut milk also shouldn’t negate the anti-inflammatory benefits of coffee. “Just don’t overdo it on your coffee servings, especially if you are jittery after drinking caffeine,” The Nutrition Twins add. “Moderation is the key.”

If you’re sensitive to caffeine or coffee, The Nutrition Twins also recommend green tea, which is extremely anti-inflammatory as well. “Although there is caffeine in green tea, it is much lower than in coffee, and the polyphenols in green tea have potent anti-inflammatory properties.”