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News flashes are posted here frequently to keep you up-to-date with the latest advances in health and longevity. We have an unparalleled track record of breaking stories about life extension advances.

Vitamin K1 supports bones

November 30 2022. The October 21, 2022, issue of Food & Function published the finding of a team from Edith Cowan University’s Nutrition and Health Innovation Research Institute and the University of Western Australia of an association between higher intake of vitamin K1 and a lower risk of hip fracture.

The study included data from 1,373 Australian women aged 70 years and older enrolled in the Perth Longitudinal Study of Aging Women. Responses to dietary questionnaires administered at the beginning of the study were analyzed for vitamin K content. During a 14.5-year follow-up period there were 153 hospitalizations due to fracture. Compared with women whose vitamin K1 intake was among the lowest 25% at less than 61 micrograms per day, women whose intake was among the highest 25% of the group at over 100 micrograms per day had a risk of hip fracture that was 31% lower and a risk of fracture-related hospitalization that was 49% lower. (Sixty micrograms per day of vitamin K has been established as the adequate intake for Australian women.)

“Our results are independent of many established factors for fracture rates, including body mass index, calcium intake, Vitamin D status and prevalent disease,” noted lead researcher Marc Sim. “Basic studies of vitamin K1 have identified a critical role in the carboxylation of the vitamin K1-dependant bone proteins such as osteocalcin, which is believed to improve bone toughness.

“A previous Edith Cowan University trial indicates dietary vitamin K1 intakes of less than 100 micrograms per day may be too low for this carboxylation,” he continued. “Vitamin K1 may also promote bone health by inhibiting various bone resorbing agents.”

“It’s another reason to follow public health guidelines, which advocate higher vegetable intake including one to two serves of green leafy vegetables — which is in-line with our study’s recommendations.”

—D Dye

Coffee, tea, protein may help lower women’s hip fracture risk

November 28 2022. Research reported in Clinical Nutrition on November 9, 2022, found a reduction in the risk of hip fracture among women with greater intake of protein, coffee or tea.

The team examined data from 26,318 participants in the Women’s Cohort Study, a prospective study that enrolled women aged 35–69 years between 1995 and 1998. Dietary questionnaires provided information concerning food and beverage intake.

During a median follow-up of 22.3 years, 822 hip fractures occurred. The team found a 14% reduction in the risk of hip fracture in association with a 25 gram per day increase in protein from any source. Among women who were underweight, the risk associated with a 25 gram per day protein increase was 45% lower.

Each cup of coffee or tea consumed was associated with a 4% lower hip fracture risk. Authors James Webster and colleagues at the University of Leeds explained that coffee and tea are high in polyphenols and phytoestrogens, especially catechins, which may enhance the activity of bone-building cells known as osteoblasts and suppress the activity of osteoclasts (which break down bone) by lowering oxidative stress. The result is greater bone mineral density and less fracture risk.

“Hip fracture can often lead to other chronic illnesses, loss of independence, and premature death,” noted Webster, who is a doctoral researcher in the School of Food Science and Nutrition at the University of Leeds. “This study is one of the first to investigate relationships between food and nutrient intakes and risk of hip fracture, with hip fractures accurately identified through hospital records. The results highlight which aspects of diet may be useful tools in reducing hip fracture risk in women, with evidence of links between higher protein, tea and coffee intakes and a reduced risk.”

—D Dye

More on flavonoids

November 25 2022.Findings from a study reported in the February 14, 2023, issue of the journal Neurology® revealed that consuming more of a type of antioxidant flavonoid known as flavonols was associated with a slower rate of cognitive decline among older men and women in comparison with consuming a low amount.

Flavonoids, a family of compounds that occur in plants, have been associated with numerous health benefits.

The study involved 961 dementia-free participants in the Rush Memory and Aging Project at Rush University in Chicago whose age averaged 81 years. Responses to yearly dietary questionnaires administered during a 6.9-year average follow-up period provided information concerning flavonol intake. Participants also completed annual cognitive and memory tests.

Flavonol intake averaged 10 milligrams (mg) per day among study participants in comparison with an average of approximately 16 mg to 20 mg per day among US adults. Global cognitive test scores of those whose intake of flavonols was among the highest 20% of participants indicated a slower rate of decline during follow-up than participants whose intake was among the lowest 20%. When individual flavonols were evaluated, participants among the highest intake of kaempferol and quercetin exhibited slower rates of cognitive decline, with kaempferol, found in significant amounts in kale, beans, tea, spinach and broccoli, being associated with the greatest benefit.

Researchers Thomas Monroe Holland, MD, MS, of Rush University Medical Center and colleagues attributed the cognitive benefit revealed in this study to flavonols’ antioxidant and anti-inflammatory properties. “It’s exciting that our study shows making specific diet choices may lead to a slower rate of cognitive decline,” Dr Holland stated. “Something as simple as eating more fruits and vegetables and drinking more tea is an easy way for people to take an active role in maintaining their brain health.”

—D Dye

Greater flavonoid intake associated with less arterial calcification

November 23 2022. The December 2022 issue of Arteriosclerosis, Thrombosis, and Vascular Biology reported a study that uncovered a relationship between greater consumption of plant compounds known as flavonoids and decreased calcification in the abdominal aorta, which supplies blood to the abdominal organs and lower limbs.

Greater abdominal aortic calcification has been associated with an increased risk of stroke, heart attack and dementia.

The study included 881 participants in the Perth Longitudinal Study of Ageing Women. Dietary questionnaire responses were analyzed to determine total and individual flavonoid intake.

Women whose total flavonoid intake was among the top 25% of participants had a 36% lower risk of extensive abdominal aortic calcification than women whose intake was among the lowest 25%. Among women whose intake of individual flavonoids known as flavan-3-ols and flavonols was among the top 25%, respective risks were 39% and 38% lower.

Those who consumed 2–6 cups per day of black tea (the main source of total flavonoid intake in this study), had a 16%–42% lower risk of extensive abdominal aortic calcification than women who were not tea drinkers.

“In most populations, a small group of foods and beverages—uniquely high in flavonoids—contribute the bulk of total dietary flavonoid intake,” first author Ben Parmenter noted. “The main contributors are usually black or green tea, blueberries, strawberries, oranges, red wine, apples, raisins/grapes and dark chocolate.”

“Out of the women who don’t drink black tea, higher total non-tea flavonoid intake also appears to protect against extensive calcification of the arteries,” he continued. “This implies flavonoids from sources other than black tea may be protective against abdominal aortic calcification when tea is not consumed.”

“Abdominal aortic calcification is a major predictor of vascular disease events, and this study shows intake of flavonoids, that could protect against abdominal aortic calcification, are easily achievable in most people’s diets,” he concluded.

—D Dye

Greater niacin intake linked with lower mortality risk among cancer patients during 15-year period

November 21 2022. A study reported on November 14, 2022, in BMC Cancer found that men and women with cancer who consumed a higher amount of niacin (vitamin B3) from food or supplements had a lower risk of dying from the disease during a 15-year follow-up period than patients with lower consumption.

Researchers analyzed data from 3,504 cancer patients who participated in the National Health and Nutrition Examination Surveys (NHANES) between 1999 and 2014. NHANES is a series of interviews and physical examinations that assess nutrition and health among U.S. residents.

Interview responses obtained at enrollment provided information concerning niacin intake. During follow-up, 1,054 deaths occurred, including 342 deaths from cancer.

Among participants whose niacin intake from food was among the top 25%, the adjusted risk of mortality from all causes was 27% lower, and the risk of dying from cancer was 49% lower during follow-up compared with participants whose intake was among the lowest 25%. Each 10 mg per day increase in dietary niacin was associated with an adjusted 11% lower risk of all-cause mortality and a 19% reduction in the risk of cancer mortality.

Total daily niacin intake was 76.4 mg per day among participants who reported using niacin supplements compared to 21.4 mg per day among those who did not supplement. Cancer mortality was 52% lower among those who supplemented with niacin versus unsupplemented participants.

“Our study found that higher intake of dietary niacin was associated with lower risk of mortality from all-causes and cancer mortality,” Hongyan Ying Taizhou of First People’s Hospital in China and colleagues concluded. “The consumption of niacin had a dose-effect relationship for all-cause mortality, but not for cancer mortality. This conclusion was verified by the data of supplemental niacin consumption.”

—D Dye

Probiotics help maintain a healthy microbiome when taken with antibiotics

November 18 2022. A systematic review published on November 16, 2022, in the Journal of Medical Microbiology helps answer the question concerning whether probiotics should be taken along with antibiotics to support gut health.

Although probiotics decrease the adverse gastrointestinal effects caused by antibiotics, their ability to preserve intestinal microbial composition that is negatively impacted by antibiotic therapy is not well understood.

"Even though we haven’t come up with a single definition of what is a healthy gut microbiome, one of the constant things we observe in healthy people is that they have a higher level of diversity and more variety of bacteria in the gut,” noted review coauthor Elisa Marroquin, PhD, who is an assistant professor at Texas Christian University.

“Like in a human community, we need people that have different professions because we don’t all know how to do every single job,” she explained. “And so, the same happens with bacteria. We need lots of different gut bacteria that know how to do different things.”

While it is well known that antibiotics destroy some beneficial intestinal microorganisms, some healthcare professionals have expressed a concern that administering probiotics to antibiotic-treated patients could further alter the established gut microbe balance.

The review included 29 studies published during a 7-year period. The authors concluded that consuming probiotics with antibiotics can prevent or reduce some changes caused by antibiotics to the microbiome. “When participants take antibiotics, we see several consistent changes in some bacterial species,” Dr Marroquin observed. “But when treatment was combined with probiotics, the majority of those changes were less pronounced and some changes were completely prevented.”

"Considering the human data available up to this point, there does not seem to be a reason to withhold a prescription of probiotics when antibiotics are prescribed.”

—D Dye

Hibiscus compound shows anti-Alzheimer disease activity

November 16 2022. A report published on October 21, 2022 in Alzheimer’s Research & Therapy revealed that gossypetin, a flavonoid occurring in the calyx of the hibiscus flower, activates a process that reduces brain accumulation of amyloid beta, a protein that clumps to form toxic brain plaques in people with Alzheimer disease.

Gossypetin has been reported to have antioxidant, antiatherosclerotic and anticancer effects. Earlier research had suggested a benefit for gossypetin, which is structurally similar to quercetin, against the aggregation of amyloid beta and tau proteins that occurs in Alzheimer disease. However, gossypetin’s action in animal models of the disease had not been evaluated.

Acting on that knowledge, researchers at Pohang University of Science and Technology administered gossypetin or a control substance to mice that were bred to develop a condition similar to that of Alzheimer disease in humans. After 13 weeks of daily treatment, mice that received the flavonoid had less amyloid beta in the brain’s hippocampus (an area involved in memory and learning) and cortex in comparison with the control mice. Gossypetin-treated animals also demonstrated better spatial learning and memory than untreated mice.

Rather than affecting the production of amyloid beta, the research team found that gossypetin helped clear it by enhancing the scavenging ability of the brain’s immune cells, which are known as microglia. Microglia normally consume amyloid beta but can become exhausted by continual exposure, which leads to a chronic damaging inflammatory reaction.

Further investigation determined that gossypetin supported the expression of genes associated with microglial amyloid beta clearance.

“We have confirmed that removing amyloid beta aggregates deposited in the brain is effective in preventing and treating dementia,” first author Kyong-Tai Kim concluded. “Gossypetin from hibiscus will contribute to the development of a safe and affordable drug for patients suffering from Alzheimer disease.”

—D Dye

Green tea, resveratrol help prevent Alzheimer plaque formation in brain model

November 14 2022.The June 2022 issue of Free Radical Biology and Medicine reported a protective effect for green tea catechins and resveratrol in brain cells infected with herpes simplex virus-1, the virus responsible for cold sores that has been shown to induce amyloid beta plaques that characterize Alzheimer disease in laboratory research.

“While previous reports have suggested these compounds as having potential neuroprotective properties, this is the first study to screen them using a human 3D cortical tissue model of Alzheimer disease representing physiologically relevant features of the disease,” the authors announced.

The Tufts University team screened 21 medications and supplements by administering them concurrently with herpes simplex virus-1 to cultured human brain tissue. Green tea catechins, resveratrol, metformin and a form of choline known as citicoline were found to help reduce amyloid beta plaque formation without antiviral effects in infected cells in comparison with infected cells that received no treatment.

Green tea and resveratrol also protected against herpes virus-induced impairments in neuron signaling, with minimal toxicity.

“We hoped to find compounds that would be harmless and show some level of efficacy,” stated researcher Dana M. Cairns, PhD, of Tufts University School of Engineering’s Kaplan Lab. “We got lucky that some of these showed some pretty strong efficacy.”

Dr. Cairns added that a positive finding in the lab “doesn’t always necessarily translate to what you might see in a patient.” Some compounds that show benefits in laboratory models may have low absorption or a poor ability to cross the blood-brain barrier.

“While it is empowering to be able to take measures like these to potentially prevent neurodegeneration in the future, it is also important to consult with your health-care provider before making any major changes to your diet,” she advised.

—D Dye

Need more motivation? Glutathione, NAC may be the answer

November 11 2022. “Do differences in metabolites in the brain affect our capacity for motivation?” asked Carmen Sandi, PhD, of Ecole Polytechnique Fédérale de Lausanne. “If that is the case, could nutritional interventions that can affect metabolite levels be an effective vehicle to improve motivated performance?”

To answer these questions, Dr Sandi and colleagues focused on an area of the brain known as the nucleus accumbens, known to play a role in reward and motivation functions. Acting on the knowledge that the brain is subject to continual metabolism-induced oxidative stress, they used proton magnetic resonance spectroscopy to measure levels of the antioxidant metabolite glutathione in the nucleus accumbens of humans and rats and compared these levels to performance in effort-related tasks that assessed motivation.

The team found a correlation between higher nucleus accumbens levels of glutathione and better motivation in task performance. When the researchers injected animals with a glutathione blocker, poorer reward-incentivized task performance was observed, indicating reduced motivation. Giving the animals the glutathione precursor N-acetylcysteine increased glutathione in the nucleus accumbens and improved performance.

“N-acetylcysteine, the nutritional supplement that we gave in our study can also be synthesized in the body from its precursor cysteine,” Dr Sandi stated. “Cysteine is contained in ‘high-protein foods’, such as meat, chicken, fish or seafood. Other sources with lower content are eggs, whole-grain foods such as breads and cereals, and some vegetables.”

“Of course, there are other ways beyond N-acetylcysteine to increase glutathione levels in the body, but how they relate to levels in the brain – and particularly in the nucleus accumbens – is largely unknown,” she continued. “Our study represents a proof of principle that dietary N-acetylcysteine can increase brain glutathione levels and facilitate effortful behavior.”

The findings were published on November 8, 2022, in eLife.

—D Dye

Hops may help lower Alzheimer disease risk

November 9 2022. Hops, the plant whose flowers are used to make beer, could have a future in the prevention of Alzheimer disease according to research reported on October 25, 2022 in the journal ACS Chemical Neuroscience.

“The search for natural compounds, whose intake through diet can help prevent the main biochemical mechanisms responsible for Alzheimer disease onset, led us to screen hops, one of the main ingredients of beer,” Alessandro Palmioli of the University of Milano-Bicocca and colleagues wrote.

Acting on other positive findings for hops, the team identified feruloyl and p-coumaroylquinic acids, flavan-3-ol glycosides and procyanidins as compounds responsible for the plant’s neuroprotective action. These molecules interacted with amyloid-beta (a substance that forms sticky plaques in the brains of Alzheimer disease patients), to prevent it from forming fibrils and becoming toxic. Hops extracts were also found to prevent cell death by inhibiting oxidative stress and inducing autophagy, a process by which cells break down and destroy old or damaged proteins or other substances. The Tettnang variety of hops proved to be the most successful of the four varieties tested.

In a roundworm model of Alzheimer disease that was bred to produce amyloid-beta 3-42, hops extract helped protect against paralysis induced by the disease.

“The identification of natural compounds or natural mixtures, such as nutraceuticals, exploitable for the development of preventive strategies against Alzheimer disease (and other neurodegenerative diseases) appears as a better alternative to the treatment of symptoms, as the neuronal damage associated with the disease is irreversible,” the authors remarked. “Our results show that hop is a source of bioactive molecules with synergistic and multitarget activity against the early events underlying Alzheimer disease development. We can therefore think of its use for the preparation of nutraceuticals useful for the prevention of this pathology.”

—D Dye

Lower risk of aspirin-induced GI bleeding in antibiotic-treated patients

November 7 2022. Results from a trial reported on November 3, 2022, in The Lancet revealed a protective effect for antibiotic treatment of the bacterium Helicobacter pylori (H. pylori) against the risk of gastrointestinal bleeding caused by aspirin.

Many people who are at high risk of stroke or heart attack use prophylactic aspirin due to its ability to thin the blood; however, this blood-thinning effect can result in bleeding from peptic ulcers caused by H. pylori infection.

The Helicobacter Eradication Aspirin Trial (HEAT) included 5,352 men and women aged 60 and older who were using a daily aspirin dose of 325 milligrams or less and had a positive breath test for H. pylori. The study excluded individuals who were using stomach-protective medications. Participants received a placebo or a combination of drugs to treat H. pylori infection twice per day for 1 week. The group was followed for up to 7 years during which any hospitalizations or deaths caused by probable or definite bleeding from peptic ulcers were ascertained.

During the first 2.5 years of follow-up, the risk of peptic ulcer bleeds was 65% lower among participants treated with antibiotics compared to the placebo group. The first case of hospitalization for bleeding ulcers occurred 6 days after the beginning of the trial in the placebo group and after 525 days in the antibiotic-treated group.

“Aspirin has many benefits in terms of reducing the risk of heart attacks and strokes in people at increased risk,” first author Chris Hawkey noted. “The HEAT trial is the largest UK-based study of its kind, and we are pleased that the findings have shown that ulcer bleeding can be significantly reduced following a one-week course of antibiotics. The long-term implications of the results are encouraging in terms of safe prescribing.”

—D Dye

Zinc supplementation associated with higher levels of brain growth factor

November 4 2022. A review and meta-analysis of randomized, controlled trials affirmed an association between supplementing with zinc and higher circulating levels of brain-derived neurotrophic factor (BDNF). Brain-derived neurotrophic factor plays a positive role in the survival of brain cells known as neurons. A reduction in BDNF expression occurs in Alzheimer and Parkinson diseases, multiple sclerosis and amyotrophic lateral sclerosis. Antidepressants and anthocyanin supplements have been shown to increase BDNF gene expression, and serum or plasma levels have been elevated by exercise and omega-3 fatty acid, resveratrol or zinc supplementation.

The research was reported on September 20, 2022, in the International Journal of Preventive Medicine.

For their review and meta-analysis, Fahimeh Agh of Iran University of Medical Sciences and colleagues identified four trials that evaluated the effects of zinc supplements on serum or plasma BDNF levels among 185. Zinc dosages ranged from 25–30 milligrams per day given for 84–90 days.

Pooled results of the trials found significantly higher BDNF levels among participants who received zinc compared with participants in the control groups. The increase in BDNF was significant at 30 milligram doses (which were used in 3 trials) and at all trial durations. Among the 3 trials that analyzed serum zinc levels, participants who were given zinc supplements had significantly increased zinc levels in comparison with the control participants.

“A large body of evidence indicated BDNF as an important predictive factor for following the beginning, progress and cure of brain disorders due to its main role in brain neurogenesis and neuroplasticity,” Agh and her associates wrote.

“Increased circulating levels of BDNF as a result of zinc supplementation suggest that zinc supplementation may be a safe and effective strategy to counteract neurodegenerative diseases that are correlated with low BDNF levels,” they concluded.

—D Dye

Iron proposed as cause of heart failure in many heart attack patients

November 2 2022. A study published October 27, 2022, in Nature Communications revealed the discovery of a cause for chronic heart failure that occurs in approximately half of the people who experience a heart attack.

“For the first time, we have identified a root cause of chronic heart failure following a heart attack,” lead researcher Rohan Dharmakumar of Indiana University School of Medicine’s Cardiovascular Institute announced.

Using large animal models, the research team found that in heart attacks in which bleeding within the heart muscle occurs upon restoration of circulation, scar tissue is gradually replaced by fat. The inability of fat to effectively propel blood from the heart can lead to heart failure in survivors of this type of heart attack. “Using noninvasive imaging, histology and molecular biology techniques, and various other technologies, we have shown that iron from red blood cells is what drives this process,” Dr Dharmakumar reported. “When we removed the iron, we reduced the amount of fat in the heart muscle. This finding establishes a pathway for clinical investigations to remedy or mitigate the effects associated with iron in hemorrhagic myocardial infarction patients.”

The finding led to a clinical trial to determine the effect of iron chelation therapy to remove excess iron in patients with hemorrhagic heart attack.

“While advances across populations have made survival after a heart attack possible for most, too many survivors suffer long-term complications like heart failure,” Indiana University’s Cardiovascular Institute physician director Subha Raman, MD noted. “Dr Dharmakumar’s breakthrough science illuminates who is at risk and why and points to an effective way to prevent these complications.”

“Thanks to a clinical trial underway being led by his team at Indiana University, I'm excited to see this treatment improve the lives of millions of heart attack survivors worldwide,” he added.

—D Dye

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