What's Hot

What's Hot

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.

  • Regular aspirin use associated with decreased pancreatic cancer risk
  • Metformin synergizes with blood pressure drug to combat cancer
  • Antioxidant enzyme protects telomeres
  • Vitamin D deficiency + high fat diet = metabolic syndrome
  • Aging may not have to proceed in one single direction
  • How metformin helps prevent cancer
  • Lutein linked to preservation of crystallized intelligence
  • Alternate day fasting eliminates one type of leukemia in mouse model
  • Trial finds improvement in lipids, glucose metabolism in women with PCOS given CoQ10
  • Down syndrome children have lower levels of CoQ10
  • Meta-analysis finds dose-response relationship between increased magnesium intake and lower diabetes risk
  • Meta-analysis affirms association of calcium supplementation with improved serum lipids

    Regular aspirin use associated with decreased pancreatic cancer risk

    metabolicSyndrome December 30 2016. On December 20, 2016, the journal Cancer Epidemiology, Biomarkers & Prevention published the results of a case-control study which found a significantly lower risk of cancer of the pancreas among regular aspirin users.

    Harvey A. Risch of Yale School of Public Health and his colleagues age-matched 761 Chinese patients diagnosed pancreatic cancer from 2006-2011 with 794 control subjects. Subjects were queried concerning lifestyle and other factors, including the use of aspirin and other nonsteroidal anti-inflammatory drugs. Regular aspirin use was defined as at least one aspirin per week for three or more months.

    Subjects with pancreatic cancer had a greater frequency of diabetes, smoked more and were likelier to carry blood group A than those without the disease. Among those who reported ever having used aspirin regularly, the risk of pancreatic cancer was 46% lower in comparison with nonusers. For each cumulative year of use, risk decreased by 8%.

    The findings of the current study were similar to those obtained in a previous study by the researchers conducted in Connecticut. “We observed a significant inverse relationship between aspirin use and risk of pancreatic cancer in a large representative sample of Chinese individuals,” Dr Risch and associates reported. “The pattern of risk reduction was very similar to that seen in other recent studies in the United States and elsewhere. Although the choice to use aspirin for disease prophylaxis generally depends upon evaluated risks of cardiovascular disease, colorectal cancer, etc., it is likely that such use at least does not increase risk of pancreatic cancer and very probably appreciably lowers it.”

    —D Dye


    Metformin synergizes with blood pressure drug to combat cancer

    metabolicSyndrome December 28 2016. The December 2016 issue of Science Advances reported that combining the antidiabetic drug metformin with the antihypertensive medication syrosingopine has shown effectiveness against several types of cancer

    The use of metformin has been associated with protection against cancer as well as therapeutic benefits, however, doses used to treat diabetes are too low for optimal anticancer effects. The current research found that syrosingopine sensitized cultured cancer cells to metformin and phenformin at a dose that was significantly lower than the individual toxic threshold of either compound. "For example, in samples from leukemia patients, we demonstrated that almost all tumor cells were killed by this cocktail and at doses that are actually not toxic to normal cells,” stated first author Don Benjamin of the Biozentrum of the University of Basel. "And the effect was exclusively confined to cancer cells, as the blood cells from healthy donors were insensitive to the treatment."

    The researchers, led by Professor Michael N. Hall, also of Biozentrum, found that the drug combo induced programmed cell death in promyelocytic leukemia and multiple myeloma cells. In mice with liver cancer, enlargement of the organ was reduced and the number and size of tumor nodules was decreased in association with treatment with the two drugs compared to the control animals. Two of the mice had livers that were tumor free.

    While metformin reduces blood glucose and blocks the mitochondria’s respiratory chain, syrosingopine inhibits the degradation of sugars, thereby interfering with processes that provide energy to the cells. "We have been able to show that the two known drugs lead to more profound effects on cancer cell proliferation than each drug alone," Dr Benjamin concluded. "The data from this study support the development of combination approaches for the treatment of cancer patients."

    —D Dye


    Antioxidant enzyme protects telomeres

    metabolicSyndrome December 23 2016.The journal Cell Reports published the discovery of researchers at Ecole Polytechnique Fédérale De Lausanne of an antioxidant enzyme that protects the cells' telomeres—sequences of repetitive nucleotides which, in turn, cap and protect the chromosomes. Telomeres are especially vulnerable to damage caused by oxygen radicals that are byproducts of normal metabolism.

    Joachim Lingner and colleagues identified the antioxidant enzyme peroxiredoxin 1 (PRDX1) on telomeres during the phase of the cell cycle in which the cells synthesize new DNA and duplicate its genetic material, as well as during the next phase when the cell grows before dividing. Removal of PRDX1 from the cells resulted in increased susceptibility to oxidative damage. 

    The researchers found that incorporation of an oxidatively damaged nucleotide in telomeres caused the cessation of chromosome growth. It was determined that telomerase, which builds chromosomes by elongating them, halted the growth process upon detection of the damaged nucleotide.

    "Our study links oxidative damage and telomeres, both of which have been previously linked to aging and cancer," Dr Lingner stated. "We expect that further studies of this problem will provide insights that help us understand mechanisms of cancer development, aging and inherited disease."

    —D Dye


    Vitamin D deficiency + high fat diet = metabolic syndrome

    metabolicSyndrome December 21 2016. An article appearing on November 15, 2016 in Frontiers in Physiology reports an essential role for vitamin D deficiency in the development of metabolic syndrome, a group of characteristics associated with an increased risk of diabetes and cardiovascular disease.

    Yuan-Ping Han and colleagues at Sichuan University, China divided 40 mice to receive a control diet supplemented with a sufficient amount of vitamin D3, a vitamin D deficient control diet, a high fat diet supplemented with vitamin D3, or a high fat diet that was deficient in vitamin D for 18 weeks. The team found that a high fat diet is necessary but not sufficient by itself to induce insulin resistance and fatty liver, and that “a second hit,” in the form of vitamin D deficiency, is required.

    It was demonstrated that a high fat diet alters gut bacteria, which contributes to elevated glucose and fatty liver. This imbalance is aggravated by a lack of vitamin D, which results in decreased production of antimicrobial molecules called defensins that are needed to maintain healthy intestinal flora.  In animals that received high fat, vitamin D deficient diets, oral administration of synthetic defensin improved intestinal bacteria balance.

    "We are planning a clinical study to confirm the link of vitamin D deficiency with gut bacteria disruption, and its association with metabolic syndrome," Dr Han announced.

    "Based on this study, we believe that keeping vitamin D levels high, either through sun exposure, diet or supplementation, is beneficial for prevention and treatment of metabolic syndrome," stated coauthor Stephen Pandol, of Cedars-Sinai Medical Center in Los Angeles. "A sufficient dietary vitamin D supplement can partially but significantly antagonize metabolic syndrome caused by high fat diet in mice. These are amounts equivalent to the dietary recommendations for humans."

    —D Dye


    Aging may not have to proceed in one single direction

    diabetes December 19 2016. In the December 15, 2016 issue of Cell, Salk Institute researchers describe a process whereby reprogramming cells to a younger state can reverse some of the signs of aging.

    "Our study shows that aging may not have to proceed in one single direction," stated senior author Juan Carlos Izpisua Belmonte. "It has plasticity and, with careful modulation, aging might be reversed."

    By inducing the expression of four genes known as the Yamanaka factors, any cell can become a pluripotent stem cell which, similar to an embryonic stem cell, is capable of becoming all cell types and dividing without limit. However, in whole organisms, having a large number of these cells could result in organ failure.

    In the current research, Yamanaka factors were induced for a short period of time in the skin cells of mice with the accelerated aging disease known as progeria. The cells underwent the reversal of multiple aging signs without losing their identity as skin cells.  "In other studies scientists have completely reprogrammed cells all the way back to a stem-cell-like state," stated co-first author Pradeep Reddy. "But we show, for the first time, that by expressing these factors for a short duration you can maintain the cell's identity while reversing age-associated hallmarks."

    In live mice with progeria, the same short reprogramming method resulted in younger looking animals with improved organ function, a lack of cancer and a 30% longer life span than untreated mice. The cells of the animals recovered molecular aging markers affected by progeria that are also altered by normal aging. "This work shows that epigenetic changes are at least partially driving aging," co-first author Paloma Martinez-Redondo stated.

    "Obviously, mice are not humans and we know it will be much more complex to rejuvenate a person," noted Dr Izpisua Belmonte. "But this study shows that aging is a very dynamic and plastic process, and therefore will be more amenable to therapeutic interventions than what we previously thought."

    —D Dye


    How metformin helps prevent cancer

    diabetes December 16 2016. The December 15, 2016 issue of the journal Cell published the discovery of researchers at Massachusetts General Hospital (MGH) of a mechanism for metformin in the inhibition of cancer.

    "We found that metformin reduces the traffic of molecules into and out of the nucleus - the 'information center' of the cell," reported senior author Alexander Soukas, MD, PhD, of the MGH Center for Human Genetic Research.  "Reduced nuclear traffic translates into the ability of the drug to block cancer growth and, remarkably, is also responsible for metformin's ability to extend lifespan. By shedding new light on metformin's health-promoting effects, these results offer new potential ways that we can think about treating cancer and increasing healthy aging."

    Dr Soukas and associates determined that metformin's anticancer ability is dependent upon the enzyme ACAD10 and the nuclear pore complex that permits the passage of molecules in and out of the nucleus, which are both elements of one genetic pathway. By restricting the passage of molecules through the nuclear pore, the cellular growth molecule mTORC1 is inhibited, thereby activating ACAD10 which slows cancer growth. "Amazingly, this pathway operates identically, whether in the worm or in human cancer cells," Dr Soukas observed. "Our experiments showed two very important things: if we force the nuclear pore to remain open or if we permanently shut down ACAD10, metformin can no longer block the growth of cancer cells. That suggests that the nuclear pore and ACAD10 may be manipulated in specific circumstances to prevent or even treat certain cancers."

    "What ACAD10 does is a great mystery that we are greatly interested in solving," he added. "Determining exactly how ACAD10 slows cell growth will provide additional insights into novel therapeutic targets for cancer and possibly ways to manipulate the pathway to promote healthy aging."

    —D Dye


    Lutein linked to preservation of crystallized intelligence

    diabetes December 14 2016. Research conducted at the University of Illinois Urbana-Champaign reveals an association between higher serum levels of the carotenoid lutein and better preservation of crystallized intelligence:  the ability to use knowledge and skills acquired over one’s lifetime. The findings were reported on December 6, 2016 in Frontiers in Aging Neuroscience.

    "Previous studies have found that a person's lutein status is linked to cognitive performance across the lifespan," commented lead researcher Marta Zamroziewicz. "Research also shows that lutein accumulates in the gray matter of brain regions known to underlie the preservation of cognitive function in healthy brain aging."

    The study included 76 cognitively normal men and women between the ages of 65 and 75 years. Blood samples were analyzed for serum levels of lutein and magnetic resonance imaging (MRI) measured gray matter volume in the temporal cortex. Crystallized intelligence was assessed by vocabulary and similarities tests.

    Participants whose serum lutein levels were higher performed better in the crystallized intelligence tests and had thicker gray matter in the brain’s parahippocampal cortex, indicating healthier brain aging. "Our analyses revealed that gray-matter volume of the parahippocampal cortex on the right side of the brain accounts for the relationship between lutein and crystallized intelligence," stated co-lead researcher Aron Barbey. "This offers the first clue as to which brain regions specifically play a role in the preservation of crystallized intelligence, and how factors such as diet may contribute to that relationship."

    "We can only hypothesize at this point how lutein in the diet affects brain structure," he added. "It may be that it plays an anti-inflammatory role or aids in cell-to-cell signaling. But our finding adds to the evidence suggesting that particular nutrients slow age-related declines in cognition by influencing specific features of brain aging."

    —D Dye


    Alternate day fasting eliminates one type of leukemia in mouse model

    diabetes December 12 2016. An article published on December 12, 2016 in Nature Medicine reveals the finding of University of Texas Southwestern Medical Center researchers of a potential benefit for every other day fasting in the treatment of the most common form of childhood leukemia. Cheng Cheng  Zhang and his associates found that alternate day fasting inhibited the initiation of B cell as well as T cell acute lymphoblastic leukemia (ALL) and reversed their progression. Fasting was not, however, effective in acute myeloid leukemia, which occurs more frequently in adults.

    "Strikingly, we found that in models of ALL, a regimen consisting of six cycles of one day of fasting followed by one day of feeding completely inhibited cancer development," Dr Zhang reported.  "Mice in the ALL model group that ate normally died within 59 days, while 75 percent of the fasted mice survived more than 120 days without signs of leukemia."

    Acting on the knowledge that fasting reduces leptin levels and that leptin receptors in humans with ALL exhibit weakened activity, Dr Zhang and colleagues evaluated leptin levels and leptin receptors in the mouse models. "We found that fasting decreased the levels of leptin circulating in the bloodstream as well as decreased the leptin levels in the bone marrow,” Dr Zhang revealed.

    "This study using mouse models indicates that the effects of fasting on blood cancers are type-dependent and provides a platform for identifying new targets for leukemia treatments," concluded Dr Zhang. "We also identified a mechanism responsible for the differing response to the fasting treatment.”

    "It will be important to determine whether ALL cells can become resistant to the effects of fasting," he added. "It also will be interesting to investigate whether we can find alternative ways that mimic fasting to block ALL development."

    —D Dye


    Trial finds improvement in lipids, glucose metabolism in women with PCOS given CoQ10

    diabetes December 9 2016. A double-blind trial that evaluated the effects of coenzyme Q10 (CoQ10) supplementation among women with polycystic ovary syndrome (PCOS) resulted in lower glucose, insulin, insulin resistance, and total and low density lipoprotein (LDL) cholesterol in those who received the supplement compared with a placebo group. The findings were reported on January 10, 2017 in the journal Clinical Endocrinology.

    Disordered lipids affect an estimated 70% of women with PCOS and insulin resistance is estimated to affect between 50% and 75%. In previous research, Zatollah Asemi and her associates found that giving 100 milligrams CoQ10 per day to subjects with metabolic syndrome improved markers of insulin metabolism.

    For the current study, they randomized 60 women with PCOS to receive 100 milligrams CoQ10 or a placebo daily for 12 weeks. Blood samples collected before and after the treatment period were evaluated for serum lipid levels and markers of insulin metabolism.

    Among CoQ10-supplemented participants, acne and scalp hair loss, which are prominent features of PCOS, were reduced by the end of the trial compared with the placebo group. Those in the CoQ10 group had lower fasting plasma glucose, serum insulin and insulin resistance. Total cholesterol and LDL cholesterol were also reduced.

    “To our knowledge, this trial is the first evaluating the effects of CoQ10 supplementation on glucose metabolism and lipid profiles among subjects with PCOS,” the authors announced.

    “Overall, CoQ10 supplementation for 12 weeks among subjects with PCOS had beneficial effects on glucose metabolism, serum total and LDL cholesterol levels,” they conclude. “This suggests CoQ10 supplementation may confer advantageous therapeutic potential for subjects with PCOS.”

    “Further studies, particularly among those with elevated insulin resistance, should measure gene expression related to insulin to explore the plausible mechanism and confirm our findings.”

    —D Dye


    Down syndrome children have lower levels of CoQ10

    diabetes December 7 2016. A study published on October 19, 2016 in Brazil’s Jornal de Pediatria reports the finding of researchers in Egypt of a reduction in levels of coenzyme Q10 (CoQ10) in boys and girls with Down syndrome compared to normal children. Trisomy 21, which causes Down syndrome, is the most frequently occurring chromosome anomaly, which affects up to one in 700 live births. Oxidative stress has been found to be involved in Down syndrome pathology.

    The case-control study enrolled 43 Down syndrome children between the ages of 5 and 8 years of age and 43 control subjects without the syndrome. Blood samples were analyzed for fasting blood glucose, coenzyme Q10, and interleukin 6 and tumor necrosis factor alpha (measures of inflammation). Intelligence quotient (IQ) was measured using standard testing.

    Higher body mass index, fasting blood glucose and markers of inflammation were observed in the Down syndrome children in comparison with the control group. Coenzyme Q10 levels were significantly lower, and the ratio of percent oxidized to total CoQ10 was greater. Researchers Moushira E. Zaki and colleagues at Egypt’s National Research Center also uncovered a correlation between higher CoQ10 levels and IQ scores. “The correlation of CoQ10 levels to IQ scores in Down syndrome patients signifies the CoQ10 effect on neurodevelopment that may be due to its protective role against nuclear DNA damage, in addition to its redox role,” they note.

    “The levels of interleukin-6, tumor necrosis factor-alpha, and CoQ10 in young Down syndrome patients might represent a key-contributing factor to the neurodegenerative process that culminates in Down syndrome,” the authors conclude. “Coenzyme Q10 should be considered a good supplement in young children with trisomy 21 to ameliorate the neurological symptoms.”

    —D Dye


    Meta-analysis finds dose-response relationship between increased magnesium intake and lower diabetes risk

    diabetes December 5 2016. The results of a systematic review and meta-analysis reported in Nutrients on November 19, 2016 found an association between increasing magnesium intake levels and a lower risk of type 2 diabetes.

    Xin Fang of the Karolinska Intitutet in Stockholm and colleagues selected 25 studies involving a total of 637,922 subjects for their analysis. Dietary questionnaire responses were analyzed for the amount of magnesium consumed. Magnesium intake ranged from a median of 115 milligrams per day in African American women to 478 milligrams per day in a U.S. population. Over 4.6 to 20 years of follow-up, 26,828 cases of type 2 diabetes were diagnosed.

    In comparison with the lowest magnesium consumption group in the meta-analysis population, men whose intake was higher had a 16% lower risk of developing diabetes and women had a 19% lower risk. For each 100 milligram per day increase in magnesium intake, the adjusted risk of type 2 diabetes was reduced by 8 to 13%.

    “To our knowledge, this study is the largest meta-analysis that investigated the dose-response relationship between dietary magnesium intake and type 2 diabetes risk,” the authors announce.

    “The combined data supports a role for magnesium in reducing risk of type 2 diabetes, with a statistically significant linear dose-response pattern within the reference dose range of dietary intake among Asian and US populations,” they conclude. “The evidence from Europe and black people is limited and more prospective studies are needed for the two subgroups.”

    —D Dye


    Meta-analysis affirms association of calcium supplementation with improved serum lipids

    Supplementation December 2 2016. A meta-analysis published on November 18, 2016 in the Journal of Cardiovascular Nursing concluded that supplementing with calcium with or without the addition of vitamin D was associated with a reduction in low-density lipoprotein (LDL) cholesterol and increased high-density lipoprotein (HDL) cholesterol. “Most (80%) lipid disorders can be treated with diet modification and exercise, and lifestyle interventions have been recommended as a primary intervention strategy among individuals with dyslipidemia,” write Chunlan Chen, BSN, RN, of Xuzhou Medical University and colleagues in their introduction to the article. “The potential role that dietary intake by nutritional supplements may have on lipid disorders, however, has not been well studied.”

    For their analysis, the researchers selected 22 randomized controlled trials that included a total of 4,071 participants who received a placebo or calcium with or without vitamin D. Studies were limited to those that provided information concerning changes in lipids following treatment.

    On average, calcium supplementation lowered LDL cholesterol by 4.64 milligrams per deciliter (mg/dL) and raised HDL by 1.93 mg/dL. The results were found to be consistent across calcium supplementation duration and vitamin D supplementation status.

    In their discussion of the findings, the authors note that low calcium diets can elevate circulating calcitrophic hormones that promote the influx of calcium ions into fat cells and increase lipid storage. Increasing calcium intake suppresses these hormones, resulting in a reduction in stored lipids.

    “To our knowledge, this is the first meta-analysis of the effect of calcium supplements on lipid changes,” they announce. “Calcium supplementation has beneficial effect on blood lipids. Such supplements may be useful as a nonpharmaceutical strategy in cholesterol control.”

    —D Dye


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