One would expect that each time a women carries a baby that the stress and depletion would speed up the aging process and shorten her life. At Simon Fraser University, health sciences professor Pablo Nepomnaschy and postdoctoral researcher Cindy Barha followed a group of 75 Kaqchikel Mayan women over a 13 year period. They discovered just the opposite of what they expected to find. The women who had more children had longer telomeres which is associated with a longer life span and a slower aging process. While it is true that pregnant women receive higher social support and experience an increase in the actions of the gonadal steroid estradiol, which increases during pregnancy those do not seem to offer a sufficient explanation. By combining this study with information that has been discovered from several others we have an interesting answer to the mystery.

An article published in Scientific American during December 2012 holds the key. When a mother is carrying a baby they are connected by the placenta. It acts as a conduit to carry nutrients, oxygen, wastes and other substances between the mother and the fetus. This has been known for a long time. What is new is the discovery that stem cells from the fetus also travel through the placenta passing from the unborn baby back into the mother. They implant in the mother and can live for decades in the brain, lung, thyroid, muscle, liver, heart, kidney, skin and other organs. There is even evidence that if the mother has an internal injury that some of the stem cells from her child may repair the damage. Young stem cells are very powerful for healing and especially appropriate for a mother because half of their genetic material came from her. Not only does a mother carry in her body cells of all her children, but the younger children may carry cells that traveled from the fetus to the mother and then into a different child later on. So oddly enough many women and even some men carry cells in their body that is partly from their children or siblings.

Very young stem cells are powerful and that is basically what a mother is receiving each time she carries a baby. No wonder women who have more children age at a slower rate.

References

Cindy K. Barha, Courtney W. Hanna, Katrina G. Salvante, Samantha L. Wilson, Wendy P. Robinson, Rachel M. Altman, Pablo A. Nepomnaschy. Number of Children and Telomere Length in Women: A Prospective, Longitudinal Evaluation. PLOS ONE, 2016; 11 (1): e0146424 DOI: 10.1371/journal.pone.0146424

Robert Martone Scientists Discover Children?s Cells Living in Mothers. Scientific American, 2012

Autophagy keeps the molecules in your cells in good working order. Cells make a lot of defective molecules. They misread genes, for example, and misfold proteins. Even a perfectly crafted molecule does not stay perfect for long. ?Proteins go bad with time,? said Daniel Klionsky of the University of Michigan. ?They age, and they wear out.?

In fact, as Dr. Klionsky wrote in a paper published online in Trends in Cell Biology, this cannibalism may extend our lifespan. Increasing our body?s ability to self-destruct may, paradoxically, let us live longer. ?All of a sudden, researchers in different fields are seeing a connection.?

When proteins and other molecules go bad, they can start to gum up the intricate chemical reactions on which a cell?s survival depends. The cell recognizes defective parts and tags them for destruction. Experiments on flies show the harm that can occur when cells cannot clear away the old and bring in the new. Flies that are genetically engineered with defective lysosomes start to accumulate abnormal clumps of proteins in their cells. The clumps build up especially in their neurons, which start to die as a result.

As mitochondria get old, they cast off charged molecules that can wreak havoc in a cell and lead to mutations. By gobbling up defective mitochondria, lysosomes may make cells less likely to damage their DNA.

Unfortunately, as we get older, our cells lose their cannibalistic prowess. The decline of autophagy may be an important factor in aging. Unable to clear away the cellular garbage, our bodies start to fail.

If this hypothesis turns out to be right, then it may be possible to slow the aging process by raising autophagy. It has long been known, for example, that animals that are put on a strict low-calorie diet can live much longer than animals that eat all they can. Recent research has shown that caloric restriction raises autophagy in animals and keeps it high. The animals seem to be responding to their low-calorie diet by feeding on their own cells, as they do during famines. In the process, their cells may also be clearing away more defective molecules, so that the animals age more slowly.

Our cells build two kinds of recycling factories. One kind, known as the proteasome, is a tiny cluster of proteins. It slurps up individual proteins like a child sucking a piece of spaghetti. Once inside the proteasome, the protein is chopped up into its building blocks.

For bigger demolition jobs, our cells rely on a bigger factory: a giant bubble packed with toxic enzymes, known as a lysosome. The Belgian biochemist Christian de Duve discovered lysosomes in 1955, for which he later won the Nobel Prize. Lysosomes can destroy big structures, like mitochondria, the sausage-shaped sacs in cells that generate fuel. To devour a mitochondrion, a cell first swaddles it in a shroudlike membrane, which is then transported to a lysosome. The shroud merges seamlessly into the lysosome, which then rips the mitochondrion apart. Its remains are spit back out through channels on the lysosome?s surface.

Lysosomes are versatile garbage disposals. In addition to taking in shrouded material, they can also pull in individual proteins through special portals on their surface. Lysosomes can even extend a mouthlike projection from their membrane and chew off pieces of a cell.

The shredded debris that streams out of the lysosomes is not useless waste. A cell uses the material to build new molecules, gradually recreating itself from old parts. ?Every three days, you basically have a new heart,? said Dr. Ana Maria Cuervo, a molecular biologist at Albert Einstein College of Medicine.

This self-destruction may seem like a reckless waste of time and energy. Yet it is essential for our survival, and in many different ways. Proteasomes destroy certain proteins quickly, allowing them to survive for only about half an hour. That speed allows cells to keep tight control over the concentrations of the proteins. By tweaking the rate of destruction, it can swiftly raise or lower the number of any kind of protein.

Lysosomes, which eat more slowly than proteasomes, serve different roles that are no less essential. They allow cells to continue to build new molecules even when they are not getting a steady supply of raw ingredients from the food we eat. Lysosomes also devour oily droplets and stores of starch, releasing energy that cells can use to power the construction of new molecules.

?If you don?t have a snack between lunch and dinner,? Dr. Cuervo said, ?you?re going to have to activate your lysosomes to get nutrients.?

Lysosomes become even more active if dinner never comes, and a short-term hunger turns to long-term starvation. Cells respond to famine by making only a small number of crucial molecules and using lysosomes to destroy the rest. ?When times are good, make everything,? Dr. Klionsky said. ?When times are lean, focus on what you need. You can get rid of everything else.?

This strategy for survival, known as autophagy (?eating oneself?), evolved in our ancestors over two billion years ago. Today, all animals rely on it to endure famines, as do plants, fungi and single-cell protozoa.

Autophagy?s great antiquity has helped scientists discover the genes that make it possible in humans. Rather than study starving people, they introduced mutations into yeast and then observed which strains could no longer survive without food. In many cases, the scientists discovered, the mutations that made yeast vulnerable struck genes that are involved in autophagy. They were then able to find nearly identical versions of those genes in the human genome.

The protection humans get from lysosomes is essential not just during famines. It is also vital just after birth. When babies emerge from their mothers, they need huge amounts of energy so that they can start to run their bodies on their own. But this demand comes at precisely the moment that babies stop getting food through their umbilical cord. Japanese scientists have found that lysosomes in mice kick into high gear as soon as they are born. After a day or two, as they start to nurse, the rate of autophagy drops back to normal.

When the scientists engineered mice so they could not use their lysosomes at birth, the newborn mice almost immediately died of starvation.

Some scientists are investigating how to manipulate autophagy directly. Dr. Cuervo and her colleagues, for example, have observed that in the livers of old mice, lysosomes produce fewer portals on their surface for taking in defective proteins. So they engineeredmice to produce lysosomes with more portals. They found that the altered lysosomes of the old experimental mice could clear away more defective proteins. This change allowed the livers to work better.

?These mice were like 80-year-old people, but their livers were functioning as if they were 20,? Dr. Cuervo said. ?We were very happy about that.?

Andrea Ballabio, the scientific director of Telethon Institute of Genetics and Medicine in Naples, Italy, and his colleagues have found another way to raise autophagy. By studying the activity of genes that build lysosomes, they discovered that at least 68 of the genes are switched on by a single master protein, known as TFEB.

When Dr. Ballabio and his colleagues engineered cells to make extra TFEB, the cells made more lysosomes. And each of those lysosomes became more efficient.

Researchers at Mayo Clinic increased normal mouse lifespan by up to 35% by removing senescent cells that accumulate with age and negatively impact health. The results, which appear today in Nature, demonstrate that clearance of senescent cells preserves tissue and organ function and extends lifespan without observed adverse effects.

“Cellular senescence is a biological mechanism that functions as an ’emergency brake’ used by damaged cells to stop dividing,” says Jan van Deursen, Ph.D., Chair of Biochemistry and Molecular biology at Mayo Clinic, and senior author of the paper. “While halting cell division of these old or damaged cells is important, it has been theorized that once the ’emergency brake’ has been pulled, these cells are no longer necessary.”

The immune system sweeps out the senescent cells on a regular basis, but over time becomes less effective. Senescent cells produce factors that damage adjacent cells and cause chronic inflammation, which is closely associated with frailty and age-related diseases.

Mayo Clinic researchers used a transgene that allowed for the drug-induced elimination of senescent cells from normal mice. Upon administration of a compound called AP20187, removal of senescent cells delayed the formation of tumors and reduced age-related deterioration of several organs. Median lifespan of treated mice was extended by 17 to 35 percent. They also demonstrated a healthier appearance and a reduced amount of inflammation in fat, muscle and kidney tissue.

“Senescent cells that accumulate with aging are largely bad, do bad things to your organs and tissues, and therefore shorten your life but also the healthy phase of your life,” says Dr. van Deursen. “And since you can eliminate the cells without negative side effects, it seems like therapies that will mimic our findings or our genetic model that we used to eliminate the cells like drugs or other compounds that can eliminate senescent cells would be useful for therapies against age-related disabilities or diseases or conditions.”

Darren Baker, Ph.D., a molecular biologist at Mayo Clinic, and first author on the study is also optimistic about the potential implications of the study for humans.

“The advantage of targeting senescent cells is that clearance of just 60-70 percent can have significant therapeutic effects,” says Dr. Baker. “If translatable, because senescent cells do not proliferate rapidly, a drug could efficiently and quickly eliminate enough of them to have profound impacts on health span and lifespan.”

Research Study:

Darren J. Baker, Bennett G. Childs, Matej Durik, Melinde E. Wijers, Cynthia J. Sieben, Jian Zhong, Rachel A. Saltness, Karthik B. Jeganathan, Grace Casaclang Verzosa, Abdulmohammad Pezeshki, Khashayarsha Khazaie, Jordan D. Miller, Jan M. van Deursen. Naturally occurring p16Ink4a-positive cells shorten healthy lifespan. Nature, 2016; DOI: 10.1038/nature16932

In the United States an increasing number of doctors are already using autologous stem cells in their practice. The stem cells are harvested from the adipose tissue (fat) or blood from bone marrow of the patient and then injected the same day into another part of the body. For instance many doctors inject joints like knees, hips and various parts of the spine. You can learn more about this or locate a physician at www.getprolo.com. The stem cells can also be injected intravenously into the cardiovascular system.

A Japanese researcher, Nobel laureate Shinya Yamanaka, collected genes from mature adult skin tissue and reprogrammed them to become pluripotent, which is a stem cell characteristic that means a cell is able to differentiate into multiple types of cells. This conversion process, referred to as induced pluripotent stem cells (iPSCs), means that we can take adult cells from a person with a particular disease, turn them into iPSCs, and then induce the iPSCs to turn into different types of body cells. Yamanaka?s iPSC findings show how scientists can essentially ?make any cell turn into any other type of cell and in effect move through wormholes in developmental time? to produce such things as a pancreas from skin tissue.? As a result, ?the petri dish becomes an avatar of the patient? whereby medicines can be identified “that will improve the condition of cells in the patient without having to take cells out of the petri dish and put them back in the patient.”

While harvesting “stem cells” from a patient’s blood from bone marrow or fat from liposuction has great value today neither of these procedures provides pluripotent stem cells needed for diverse tissue differentiation in a laboratory. Rather, these procedures produce mesenchymal cells, which work well for cardiovascular and orthopedic conditions because these tissues are the end organ targets for mesenchymal cells. However, they do not work well for other germ cell layer target organs, such as those produced from endoderm (incl., pancreas, liver, lungs) and ectoderm (incl., nervous system, skin).

Fortunately, there is a lesser known but more viable means for obtaining real pluripotent stem cells that merely involves a blood draw. In 2005, a study published in Minerva Biotechnologica identified stem cells in the blood. In other follow-up studies, scientists showed that such cells could, in fact, be used to regenerate not only heart tissue, but brain, lung, and pancreas as well.

In 2010, a clinical protocol was developed for harvesting, concentrating, reconstituting, and administering pluripotent stem cells obtained from autologous blood. Today the use of stem cells for clinical applications is in its infancy. Physicians still have much to learn about how to more effectively utilize pluripotent stem cells in their practice for the benefit of their patients. Such knowledge includes not only using the most appropriate source for harvesting real stem cells but in improving the means of attracting those stem cells to where they are needed and facilitating their differentiation. As more physicians implement the use of pluripotent stem cells in their practice, such as those obtained from autologous blood, we can begin accumulating the objective data needed to validate stem cells in the present and advance stem cell science into the future.

A hormone that extends lifespan in mice by 40% is produced by specialized cells in the thymus gland, according to a new study by Yale School of Medicine researchers. The team also found that increasing the levels of this hormone, called FGF21, protects against the loss of immune function that comes with age.

Published online in the Proceedings of the National Academy of Sciences on Jan. 11, the study’s findings have future implications for improving immune function in the elderly, for obesity, and for illnesses such as cancer and type-2 diabetes.

When functioning normally, the thymus produces new T cells for the immune system, but with age, the thymus becomes fatty and loses its ability to produce new T cells. This loss of new T cells in the body is one cause of increased risk of infections and certain cancers in the elderly.

Led by Vishwa Deep Dixit, professor of comparative medicine and immunobiology at Yale School of Medicine, the researchers studied transgenic mice with elevated levels of FGF21. The team knocked out the gene’s function and studied the impact of decreasing levels of FGF21 on the immune system. They found that increasing the levels of FGF21 in old mice protected the thymus from age-related fatty degeneration and increased the ability of the thymus to produce new T cells, while FGF21 deficiency accelerated the degeneration of the thymus in old mice.

“We found that FGF21 levels in thymic epithelial cells is several fold higher than in the liver therefore FGF21 acts within the thymus to promote T cell production,” said Dixit.

“Elevating the levels of FGF21 in the elderly or in cancer patients who undergo bone marrow transplantation may be an additional strategy to increase T cell production, and thus bolster immune function,” said Dixit.

Dixit added that FGF21 is produced in the liver as an endocrine hormone. Its levels increase when calories are restricted to allow fats to be burned when glucose levels are low. FGF21 is a metabolic hormone that improves insulin sensitivity and also induces weight loss.

Dixit said further studies will focus on understanding how FGF21 protects the thymus from aging, and whether elevating FGF21 pharmacologically can extend the human healthspan and lower the incidence of disease caused by age-related loss of immune function.

“We will also look to developing a way to mimic calorie restriction to enhance immune function without actually reducing caloric intake.”

Journal Source:

Yun-Hee Youm, Tamas L. Horvath, David J. Mangelsdorf, Steven A. Kliewer, Vishwa Deep Dixit. Prolongevity hormone FGF21 protects against immune senescence by delaying age-related thymic involution. Proceedings of the National Academy of Sciences, 2016; 201514511 DOI: 10.1073/pnas.1514511113

Summary:

Liver-derived metabolic hormone fibroblast growth factor 21 (FGF21) improves insulin sensitivity and extends lifespan in mice. Aging also compromises the adaptive immune system by reducing T-cell production from the thymus. In this paper, we describe a new immunological function of FGF21 as a regulator of T-cell production from thymus in aging. The overexpression of FGF21 prevents thymic lipoatrophy, which protects the mice from age-induced loss of na?ve T cells. FGF21 expression in thymic epithelial cells and signaling in thymic stromal cells support thymic function in aging. Loss of FGF21 in mice increases lethality postirradiation and delays the reconstitution of thymus. Hence, we highlight FGF21 as an immunometabolic regulator that can be harnessed to delay immune senescence.

Abstract:

Age-related thymic degeneration is associated with loss of na?ve T cells, restriction of peripheral T-cell diversity, and reduced healthspan due to lower immune competence. The mechanistic basis of age-related thymic demise is unclear, but prior evidence suggests that caloric restriction (CR) can slow thymic aging by maintaining thymic epithelial cell integrity and reducing the generation of intrathymic lipid. Here we show that the prolongevity ketogenic hormone fibroblast growth factor 21 (FGF21), a member of the endocrine FGF subfamily, is expressed in thymic stromal cells along with FGF receptors and its obligate coreceptor, ?Klotho. We found that FGF21 expression in thymus declines with age and is induced by CR. Genetic gain of FGF21 function in mice protects against age-related thymic involution with an increase in earliest thymocyte progenitors and cortical thymic epithelial cells. Importantly, FGF21 overexpression reduced intrathymic lipid, increased perithymic brown adipose tissue, and elevated thymic T-cell export and na?ve T-cell frequencies in old mice. Conversely, loss of FGF21 function in middle-aged mice accelerated thymic aging, increased lethality, and delayed T-cell reconstitution postirradiation and hematopoietic stem cell transplantation (HSCT). Collectively, FGF21 integrates metabolic and immune systems to prevent thymic injury.

Acoustics experts have created a new class of sound wave — the first in more than half a century in a breakthrough they hope could lead to a revolution in stem cell therapy.

The team at RMIT University in Melbourne, Australia, combined two different types of acoustic sound waves called bulk waves and surface waves to create a new hybrid: “surface reflected bulk waves.”

The first new class of sound wave discovered in decades, the powerful waves are gentle enough to use in biomedical devices to manipulate highly fragile stem cells without causing damage or affecting their integrity, opening new possibilities in stem cell treatment.

Dr Amgad Rezk, from RMIT’s Micro/Nano Research Laboratory, said the team was already using the discovery to dramatically improve the efficiency of an innovative new “nebuliser” that could deliver vaccines and other drugs directly to the lung.

“We have used the new sound waves to slash the time required for inhaling vaccines through the nebuliser device, from 30 minutes to as little as 30 seconds,” Rezk said.

“But our work also opens up the possibility of using stem cells more efficiently for treating lung disease, enabling us to nebulise stem cells straight into a specific site within the lung to repair damaged tissue.

“This is a real game changer for stem cell treatment in the lungs.”

The researchers are using the “surface reflected bulk waves” in a breakthrough device, dubbed HYDRA, which converts electricity passing through a piezoelectric chip into mechanical vibration, or sound waves, which in turn break liquid into a spray.

“It’s basically ‘yelling’ at the liquid so it vibrates, breaking it down into vapour,” Rezk said.

Bulk sound waves operate similar to a carpet being held at one end and shaken, resulting in the whole substrate vibrating as one entity. Surface sound waves on the other hand operate more like ocean waves rolling above a swimmer’s head.

“The combination of surface and bulk wave means they work in harmony and produce a much more powerful wave,” said Rezk, who co-authored the study with PhD researcher James Tan.

“As a result, instead of administering or nebulising medicine at around 0.2ml per minute, we did up to 5ml per minute. That’s a huge difference.”

The breakthrough HYDRA device is improving the effectiveness of a revolutionary new type of nebuliser developed at RMIT called Respite. Cheap, lightweight and portable, the advanced Respite nebuliser can deliver everything from precise drug doses to patients with asthma and cystic fibrosis, to insulin for diabetes patients, and needle-free vaccinations to infants.

In a study published Monday in the Proceedings of the National Academy of Sciences, the scientists tracked 1,000 people born in 1972-73 in the coastal city of Dunedin in New Zealand and calculated their “biological age” after their 38th birthdays based on a wide range of biomarkers. The measurements included:

?Kidneys, liver, lungs, metabolic and immune systems
?HDL cholesterol, cardiorespiratory fitness, lung function
?Length of the telomeres (protective caps at the end of chromosomes that have been found to shorten with age)
?Dental health like the condition of the gums
?Condition of the tiny blood vessels at the back of the eyes, (which are a proxy for the brain’s blood vessels)
?Cognitive function

They looked at the volunteers at age 26, 32 and 38 and found that while most of them aged at a normal pace — one year’s worth of physiological changes for each chronological year — some of them aged surprisingly slower or faster.

In fact, researchers calculated, the “biological ages” of the 38-year-olds ranged from 30 to nearly 60 years. From the report:

The fastest-aging study participants experienced two to three years of changes with the passage of a single calendar year. They tended to have worse balance and motor coordination and were physically weaker. Belsky and his colleagues said that these volunteers reported having more trouble with basic tasks like climbing stairs or carrying groceries.

Moreover, those who were aging fast also showed evidence of cognitive decline. Their IQ scores, which according to previous studies have been shown to remain relatively constant throughout a person’s life, were lower by age 38.

One particularly interesting finding of the study was that the people who were physiologically older looked older, at least according to Duke undergraduates who were asked to guess their ages from their pictures.

The study, which was funded in part by the National Institute on Aging, is significant because it looked at young adults. Most previous aging research is focused on the second half of the average person’s life, in the 50s, 60s, and 70s.

“Our findings indicate that aging processes can be quantified in people still young enough for prevention of age-related disease, opening a new door for antiaging therapies,” the researchers wrote. “The science of healthspan extension may be focused on the wrong end of the lifespan; rather than only studying old humans, geroscience should also study the young.”

Belsky said that in the future a person’s biological age could serve as a simple measure of a person’s health that may help patients better understand the battery of numbers they get from their doctors today.

“A single number would be much easier to process,” Belsky said.

He said the measurement could also help with assessing the health of a community. Right now we look at things like disease end points, new diagnoses, hospitalizations and death, but all are imperfect because they don’t give us a picture of the health of a whole person.

When Steve and Rosa Barney?s daughter Isabella, now 4, was born, the couple decided to take a preventative medical measure that felt both mysterious and hopeful: They banked their baby girl?s cord blood with a private company, thinking that its rich stem cells could be there to help treat an unforeseeable issue, such as childhood leukemia. They also considered that it might someday benefit their older son, who suffers from a motor speech disorder called childhood apraxia.

They wound up using it sooner than they thought, and in a way that totally amazed them ? for Isabella?s own apraxia, discovered at 18 months and largely turned around when she was 3, after a 15-minute, cutting-edge procedure, in which a their daughter had an infusion of her own stored cord blood. ?It was like her being born again,? says Steve, of Queens, New York, who notes that he and his wife were stunned by the results.

Cord blood banking is where the stem cells are removed from an newborn?s umbilical cord once it?s been clamped and cut. Those cells are then sent to a lab and frozen as a type of insurance, in case one day, if needed, they can be thawed and used to treat certain health conditions and diseases.

?We got on the ball a bit quicker with her,? Steve explains, having her tested and utilizing early intervention services when she was very young. But she went to preschool at 2 1/2 with ?very limited vocabulary,? he says, and, after preschool, had only about 15 words that could be understood (typically, a 3-year-old would have about 500 words at his or her disposal). Her parents dove into research about using stored cord-blood for treating apraxia, and found a cutting-edge program at Duke University, where stem-cell pioneer Dr. Joanne Kurtzberg had already overseen a handful of similar, successful treatments ? including for a 5-year-old with cerebral palsy, Grace Rosewood, who experienced vast improvements after receiving infusions of her stored cord blood as part of a clinical trial.

?We were still hesitant,? Steve recalls about taking the chance. ?One thing they don?t tell you with banking is that it?s basically a one-time use.? Still, after speaking with another parent about having success with the treatment at Duke, he says, ?it was a no-brainer for me.?

Then came the elaborate process of looking into whether or not Isabella was a good candidate. ?We look at the cord blood, as some banks get a higher quality than others, and we need make sure we have enough cells, with a minimum amount of information, plus good sterility,? says Kurtzberg ? who also runs a public cord-blood bank and Carolina Cord Blood Bank, accepting donations from moms who deliver healthy babies but who have no risks, and is the president of the new Cord Blood Association, created to harmonize education, regulation, and advocacy around the issue of cord-blood banking.

Regarding the decision of whether to bank a baby?s cord-blood privately or publicly, Kurtzberg explains, ?A mom has to know she?s really giving up her rights to the cord blood with a public donation. If it happens to be there, she can have it. There?s no risk, no cost, and is the truly altruistic choice.? Publicly donated cord blood is available to anyone, and doesn?t necessarily have to be a full match; it?s particularly useful for both children and adults who have conditions that cannot be treated with one?s own cord blood ? including some cancers, sickle cell, and metabolic disease.

Isabella received her treatment after receiving a full workup, including tests to make sure there was no genetic disease present. She checked out, and the cord blood was shipped to Duke.

The family was there for three days with their daughter, but the whole infusion process, given through an IV, took just 10 to 15 minutes, Steve says. As Kurtzberg explains, ?The child gets an IV ? sometimes the veins in the feet are easiest to access ? and they get Benadryl and a steroid to prevent reactions.? Then they infuse the cells, which have been washed in a lab, through a drip, similar to how a blood transfusion works. Duke typically does about three to four infusions a week, though that number will soon go up to 10, she says.

?After they put a needle in her foot, she slept for over an hour, and woke up smelling like a can of creamed corn, from the chemicals,? Steve recalls. ?It was the most beautiful smell you could smell.? Isabella?s speech abilities were immediately improved, he adds ? ?like night and day.? She?s now up to about 60 words, he adds, and though is still relying on extra speech-therapy services, ?the biggest thing is that she picks up new words without telling us, and that catches us by surprise all the time.?

The cost of the procedure, Kurtzberg says, averages $7,500 to $10,000, and is only sometimes covered by insurance. In the Barneys? case, the family?s insurance covered about 40 percent. ?It was very worth it,? Steve says ? especially the cord blood banking part. ?I suggest it to everybody, because you just never know.?

High consumption of trans fats such as found in foods containing hydrogenated oils is linked to worse memory according to a study among working-age men, according to research presented at the American Heart Association’s Scientific Sessions 2014.

In a recent study of approximately 1,000 healthy men, those who consumed the most trans fats showed notably worse performance on a word memory test. The strength of the association remained even after taking into consideration things like age, education, ethnicity and depression.

“Trans fats were most strongly linked to worse memory, in young and middle-aged men, during their working and career-building years,” said Beatrice A. Golomb, M.D., Ph.D., lead author and professor of medicine at the University of California-San Diego. “From a health standpoint, trans fat consumption has been linked to higher body weight, more aggression and other health problems. As I tell patients, while trans fats increase the shelf life of foods, they reduce the shelf life of people.”

Golomb and her coauthor studied adults including men age 20 or older and postmenopausal women. Participants completed a dietary questionnaire, from which the researchers estimated participants’ trans fat consumption. To assess memory, researchers presented participants with a series of 104 cards showing words. Participants had to state whether each word was new or a word duplicated from a prior card.

?Among men under age 45, those who ate more trans fats showed notably worse performance on the word memory test. The strength of the association remained even after taking into consideration things like age, education, ethnicity and mood.

?Each additional gram a day of trans fats consumed was associated with an estimated 0.76 fewer words correctly recalled.

?For those eating the highest amounts of trans fats, this translated to an estimated 11 fewer words (a more than 10 percent reduction in words remembered), compared to adults who ate the least trans fat. (The average number of words correctly recalled was 86.)

“Foods have different effects on oxidative stress and cell energy,” Golomb said. In a previous study, we found chocolate, which is rich in antioxidants and positively impacts cell energy, is linked to better word memory in young to middle-aged adults. In this study, we looked at whether trans fats, which are prooxidant and linked adversely to cell energy, might show the opposite effect. And they did.”

Industrial trans fats are artificially produced to turn liquid oils into solids at room temperature and extend food shelf life. They can be found in margarines, fast foods, baked goods, snack foods, frozen pizza, coffee creamers and some refrigerated doughs. The Food and Drug Administration is taking further steps to reduce the amount of artificial trans fats in the U.S. food supply.

Analyses in younger women are needed to determine whether effects extend to this group, Golomb said.