Organs are a Mix of New and Old Cells

cellsIt was once thought that neurons and possibly heart cells, were the oldest cells in the human body. However, researchers have discovered that the mouse liver, brain and pancreas contain populations of proteins and cells with very long lifespans with some as old as neurons.

The findings at the Salk Institute demonstrating age mosaicism could be applied to nearly any body tissue for providing valuable information about the lifelong function of non dividing cells and how cells lose control over the integrity and control of proteins and important cell structures during the aging process.

The team was very surprised to discover cellular structures that are as old as the organism where they reside. This discovery suggests even greater cellular complexity than was previously imagined. It provides intriguing implications about how we think about the aging process of organs such as the heart, pancreas and brain.

Most brain neurons do not divide in adulthood and therefore experience a long lifespan and then age related decline. However, due to technical limitations, the life of cells outside the brain has been difficult to determine. Researchers have wondered how old the cells are in an organism.

There has been the general idea that neurons are old yet other cells in the human body are relatively young and will regenerate throughout the lifetime of the organism. The research team proceeded to see if there was the possibility that certain organs also have cells that are as long lived as brain neurons.

The researchers knew that most neurons will not be replaced during lifespan. They utilized them as an age baseline for comparison to other non dividing cells. They combined electron isotope labeling with a hybrid imaging method so they could visualize and then quantify protein and cell age and turnover in the liver, pancreas and brain in both old and young rodents.

To validate the method, the team initially determined the age of the neurons and found that they were as old as the organism. However, the cells that line blood vessels, known as endothelial cells, were also as old as the neurons. This means that some of the non neuronal cells do not replace or replicate themselves during lifespan.

The pancreas which is an organ whose function it is to maintain blood sugar levels and also secrete digestive enzymes, also showed cells at different ages. A small portion of the pancreas appeared as a puzzle of interconnected old and young cells. Some of the beta cells which release insulin replicated through lifetime and were relatively young. However, some did not divide and were long lived which is similar to neurons. Another type of cell called delta cells, did not divide at all. The pancreas is a great example of age mosaicism or a population of identical cells which are distinguished by their lifespans.

Previous research has suggested the liver has the ability to regenerate during adulthood so the team chose this organ with the expectation of seeing relatively young liver cells. However, the vast majority of liver cells in healthy adult mice were as old as the mice while cells which line blood vessels and stellate like cells, were much shorter lived. The liver also demonstrated ago moscaicism which indicates potential new paths of regenerative research of this organ.

Due to new visualizing technologies, the team was able to pinpoint the age of cells and their supra molecular complexes more precisely that before. This opens new paths for studying tissues, cells and organs in both normal and in diseased states.

By determining the age of sub cellular structures and cells in adult organisms, new insights into cell repair mechanisms and maintenance and the impact of cumulative changes during adulthood on development of diseases and health can occur.

The ultimate goal is to be able to utilize these mechanisms in an effort to delay and prevent age related decline of organs with limited cell renewal. The team plans to decipher the differences in lifespans for lipids and nucleic acids and also to understand how age mosaicism relates to diseases and overall health.

To view the original scientific study click here: Age Mosaicism across Multiple Scales in Adult Tissues.

How the Brain Affects Aging

A new discovery by researchers at the Albert Einstein College of Medicine has shown that stem cells found in the brain’s hypothalamus affect how fast our body’s age. The discovery which was made in mice, could possibly lead to new strategies for defending against age related diseases and even extending lifespan.

The hypothalamus regulates critical processes including development, growth, metabolism and reproduction. Einstein researchers made the surprising discovery that it also regulates aging throughout the entire body. Now, they have pinpointed the exact cells in the hypothalamus that control the process of aging. These cells are a tiny population of adult neural stem cells which are known to be responsible for the formation of new brain neurons.

The research has shown that the number of hypothalamic neural stem cells will naturally decline throughout the life of an animal. This decline will accelerate with aging. The team also discovered that the effects of this stem cell loss are not irreversible. Through replenishing these stem cell or the molecules they produce, it is possible to slow down and even reverse a variety of the aspects associated with aging within the body.

To study whether stem cells found in the hypothalamus hold the key to aging, the team first looked at the fate of the stem cells as healthy mice aged. The number of these stem cells did begin to decline when the mice reached almost 10 months of age which is quit a few months before the normal signs of aging start to appear. By old age which is about two years in mice, most of these stem cells were gone.

The team then wanted to learn whether the progressive loss of these stem cells was actually causing the aging and was not only associated with it. They observed what happened after they selectively disrupted these stem cells in the hypothalamus in middle aged mice. The disruption greatly accelerated the aging compared with control mice. The mice with the disrupted stem cells also died earlier than what would be normal.

The question became, could adding stem cells to the hypothalamus actually counteract aging? The team sought to answer that question by injecting hypothalamic stem cells in the brains of the middle aged mice whose stem cells were destroyed along with injecting the brains of the normal older mice. In both groups of mice the treatment either slowed or reserved a variety of measures of aging.

The team found that the hypothalamic stem cells appeared to exert their anti aging effects by the release of molecules called microRNAs. Rather than being involved in the synthesis of protein, they instead played key roles in regulating gene expression. MicroRNAs are contained inside tiny particles known as exosomes which stem cells in the hypothalamus release into the cerebrospinal fluid of mice.

The team then extracted microRNA containing exosomes from the hypothalamic stem cells and injected them into the cerebrospinal fluid of two different groups of mice…middle aged mice whose hypothalamic stem cells were destroyed and the normal middle aged mice. The treatment showed significant slowing of aging in both groups of mice through a measure of tissue analysis and also behavioral testing which involved assessing any changes in the mice’s coordination, muscle endurance, cognitive ability and social behavior.

They are now working at identifying the particular populations of the microRNAs and even other factors secreted by these stem cells which are responsible for the anti aging effects. This is potentially a first step to possibly slowing down the aging process and also treating a variety of age related diseases.

To view the original scientific study click below

Hypothalamic stem cells control ageing speed partly through exosomal miRNAs

Diabetes Prevention with Intermittent Fasting

Scientists at the German Institute of Human Nutrition have found through research on mice that have been put on intermittent fasting, have exhibited lower pancreatic fat. Pancreatic fat has been shown to contribute to the development of type 2 Diabetes. This type of fasting is known to improve the sensitivity to the glucose lowering hormone insulin and can also protect against fatty liver.

Fatty liver has been previously investigated and is known as a frequently occurring disease. However, very little has been known in regards to excess weight induced accumulation of fat in the pancreas and its effects on the onset of type 2 diabetes.

The team has now discovered that mice who are overweight and prone to diabetes have a high accumulation of fat cells in their pancreas. Mice that are resistant to diabetes because of their genetic make up and despite their excessive weight, had hardly any fat cells in their pancreas. Instead they had fat deposits in their liver. Accumulations of fat outside the fat tissue in the muscles, liver and even bones, have a negative effect on those organs and the whole body. What impact fat cells might have within the pancreas has not been previously clear.

The research team divided the animals that were overweight and prone to diabetes into two groups. The first group of mice were allowed to eat as much they wanted and whenever they wanted. The second group of mice underwent a regime of intermittent fasting. One day they were given unlimited chow and the following day they were not fed at all.

After five weeks, the team noted differences in the pancreas of the mice. An accumulation of fat cells were found in the first group. In the second group however, there were hardly any deposits of fat in the pancreas.

To find out how fat cells could impair pancreas function, the team isolated adipocyte (a cell specialized for the storage of fat and found in connective tissue) precursor cells taken from the mice’ pancreas for the first time and then allowed them to differentiate into mature fat cells. If these mature fat cells were then cultivated together with the Langerhans islets of the pancreas, the islets beta cells increasingly secreted insulin. The team suspects that an increase secretion of insulin causes the Langerhans islets of animals prone to diabetes to deplete more quickly and cease functioning completely after time.

The islets of Langerhans are islet like accumulations of hormone producing cells within the pancreas. A healthy adult has approximately one million Langerhans islets. Beta cells produce the blood glucose lowering hormone known as insulin and they make up about 75 to 80% of the islet cells. When blood glucose levels are elevated, these beta cells secrete insulin into the blood steam to normalize levels.

The most current data suggests that not only should liver fat be reduced to help prevent the onset of type 2 diabetes, but under certain genetic conditions, an accumulation of fat in the pancreas might also play a decisive role in the development of this disease.

Intermittent fasting just might be a very promising therapeutic approach. Intermittent fasting is easy to integrate into daily life, does not require drugs and is non invasive. Intermittent fasting simply involves not eating during certain times of the day. However, black coffee, water and unsweetened tea can be consumed around the clock. Fasting can last between 16 and 24 hours or alternatively a maximum of 500 to 600 calories can be consumed on two days within a week.

One of best forms of intermittent fasting is the 16 and 8 method. This method involves eating only within an eight hour window during a day then fasting for the other 16 hours. One meal which is typically breakfast is omitted.

To view the original scientific study click below

Pancreatic adipocytes mediate hypersecretion of insulin in diabetes-susceptible mice

Enhance Brain Function with Just a Short Bout of Exercise

Short bouts of exercise has been found to directly boost gene function which increases the connections between neurons in the hippocampus. This part of the brain is associated with memory and learning. Not only is exercise good for health, but according to recent research it can also help make you smarter!

Neuroscientists at Oregon Health & Science University designed research using mice that specifically measured their brain’s response to just single bouts of exercise. Mice that were normally sedentary were placed on running wheels for short periods. They ran a few kilometers in a two hour time period.

The results of the study found that short term bouts of exercise similar to the human equivalent of 4,000 steps or a weekly game of basketball, promoted synapses increases in the hippocampus. The team made the discovery through analyzing genes that increased in single neurons which were activated during exercise.

A particular gene stood out, the Mtss 1L gene. This gene has been ignored in previous studies of the brain. This gene encodes a protein which causes the cell membrane to bend. When this gene is activated through short bursts of exercise, it will promote small neuron growths known as dendritic spines which is the site where synapses form.

The study has shown that an acute burst of exercise can prime the brain for learning. For the next stage of their research, the scientists plan to pair acute bursts of exercise with learning tasks to more fully understand the impact on memory and learning.

To view the original scientific study click below

Exercise-induced enhancement of synaptic function triggered by the inverse BAR protein, Mtss1L

Helping Bones Heal Faster

A team at the University of Illinois and the University of Pennsylvania created a new technique which uses flexible implantable bone stabilizing plates and stem cells to assist in faster healing of bone defects and large breaks. This new technique allows stem cells which are applied to break sites to experience a level of mechanical stress which they also do in developing embryos.

The forces used can help encourage stem cells to differentiate into bone and cartilage in addition to encouraging other cells within bones to regenerate. Stem cells require environmental cues to be able to differentiate into cells which make up unique tissues. Stem cells which give rise to cartilage and bone are subject to mechanical type forces during healing and development.

As a bone heals, stem cells in the bone marrow close to the break site initially become cartilage cells and at a later time bone cells. This ultimately knits the bone together. When large gaps occur between deformed and broken bones, applying more stem cells to the break sites can assist in the bones healing faster. This is achieved by either stimulating bone formation by neighboring cells or by actively participating in the regenerative process.

However, to use stem cells for the purpose of bone regeneration, they have to be delivered to the broken and defect site and then differentiate appropriately to begin repair stimulation. The team developed a unique preparation of the stem cells which can be handled and also manipulated easily for implantation and also supports the events of cellular differentiation which occur in the development of embryonic bone.

In the preparation process, stem cells are first cultured so they will link to each other to form either plugs or sheets. This preparation also contains gelatin microparticles which are loaded with growth factors which will help these stem cells differentiate. The plugs or sheets can be manipulated and then implanted which reduces the tendency of cells drifting away. These materials are called condensates.

In earlier studies, the team employed condensates in rodent models to help heal defects in the skull. They noticed the condensates remained in place and were then able to improve the extent and rate of bone regeneration.

Recently, the researchers teamed up with an assistant professor of orthopedic surgery and bioengineering at Penn Medicine to take their idea a step further. They have developed a unique and flexible fixator. Fixators are typically stiff metal bars or plates which are used to stabilize bones at their break sites. This type of fixator minimizes the degree of mechanical stress breaks will experience during the healing process.

The new flexible fixator would allow the stem cells in the condensates to experience the compressive forces which are critical to stimulating enhanced bone and cartilage formation. The team used a rat model to see how the mechanical forces would present within defects of the bone which affected the ability of the condensates to contribute to bone regeneration.

When they used condensate sheets together with the flexible fixator in rats with a femur defect, they observed there was enhanced healing and the bones actually had better mechanical function compared to control rats which received condensates and the traditional stiff fixators.

Other techniques and devices that could be developed from this new research could also help in the way physical therapy is employed after injury. The findings support the emerging paradigm called regenerative rehabilitation which is a concept that marries principles from regenerative medicine and physical therapy. The goal is to understand how mechanical stimuli influences the behavior of cells to achieve better patient outcomes without additional devices and drugs.

To view the original scientific study click below

Recapitulating bone development for tissue regeneration through engineered mesenchymal condensations and mechanical cues.

Losing Weight with Coffee

A new discovery by scientists at the University of Nottingham indicates drinking a cup of coffee can actually stimulate brown fat. Brown fat is the body’s fat fighting defense which just might be the key to tackling diabetes and obesity.

The study published in Scientific Reports, is one of the first ones to be tested in humans in an effort to discover components which might have a direct effect on the functions of brown fat. This important part of the body plays a significant role in how fast we burn calories as energy.

BAT (brown fat tissue) is one of the two types of fat that is found in some mammals and humans. It was initially attributed only to hibernating mammals and babies. It has been discovered in recent years that adults too can have brown fat with its main function being generating body fat by burning calories. This is different from white fat which is a result of excess calorie storage. People that have a lower body mass index thus have a higher amount of the brown fat.

Professor Michael Symonds who co directed the study says that brown fat works in different ways than other types of fat in the body. It produces heat by burning fat and sugar often as a response to cold. By increasing its activity, blood sugar control is improved in addition to the improvement of blood lipid levels and the extra calories that are burned help with weight loss. However, until this study no one has been able to find an acceptable way to stimulate brown fat activity in humans.

The current study is the first one to show that something like coffee can have a direct effect on brown fat functions. Since obesity is a major health concern, the potential implications of the studies results could be big. This also includes potential help for the growing diabetes epidemic.

The researchers began with a series of stem cell studies as a way to see if caffeine could stimulate brown fat. When they found the correct dose, they moved to studies in humans to see if the earlier results would be similar.

They used a thermal imaging technique that had previously been pioneered to follow the body’s reserves of brown fat. This non invasive technique enabled them to find brown fat and then assess its ability to produce heat.

From previous research the team knew that brown fat is mostly located in the region of the neck. They were able to image a person right after they had a cup of coffee to see if the brown fat got hotter.

The imaging results were positive and the team now needs to ascertain whether the caffeine is one of the coffee ingredients which is acting as the resulting stimulus or if there is a different component helping with activating the brown fat.

The team is now looking at caffeine supplements for testing to see if the effect is similar. Once they have confirmed which component activated the stimulus, it could potentially be employed as part of a weight management treatment or as part of a glucose regulation treatment to help prevent the development of diabetes.

To view the original scientific study click below

Caffeine exposure induces browning features in adipose tissue in vitro and in vivo.

Heavily Processed Foods and Health Issues

A new small scale controlled research trial, the first of its kind, has linked consumption of ultra processed foods to overeating and weight gain. People who eat these kinds of foods typically eat more calories when compared to eating a minimally processed diet.

Observational studies previously conducted looked at large groups of people had indicated associations between health problems and diets high in processed foods. However, these studies randomly instructed people to consume specific foods and then measured results. Researchers could not say for sure if the processed foods were problematic on their own or people had a variety of health problems due to other reasons.

The study conducted at the NIH’s National Institute of Diabetes and Digestive and Kidney Diseases, involved 20 adult volunteers. This was the first randomized controlled trial to examine effects of an ultra processed foods diet which are defined by the NOVA classification system. Ultra processed foods are foods that have ingredients predominantly found in industrial food manufacturing. This includes foods such as high fructose corn syrup, hydrogenated oils, emulsifiers and flavoring agents.

The people involved in the study were healthy volunteers and included 10 male and 10 female participants. They were all admitted to the NIH Clinical Center for one continuous month. In random order for two weeks, they were provided with meals made up of minimally processed foods or ultra processed foods.

An ultra processed breakfast would have included bagel with cream cheese and turkey bacon. The unprocessed breakfast would have included oatmeal with walnuts bananas and skim milk. The difference between the two diets is very subtle on the surface as both diets included eggs, beans, cereals and pastas. However, the unprocessed foods included ingredients that were fresher with no added preservatives or additives and included unrefined ingredients and whole foods.

Both diets had the same quantities of sugars, calories, fiber, fat and carbohydrates. Participants were allowed to eat as much or as little as they preferred during an hour long period. Although the current study involved just 20 adults, the results from the tightly controlled experiment indicated a consistent and clear difference between the two diets.

The research team measured changes in the participant’s appetite, insulin sensitivity, glucose and a variety of other physical and metabolic factors.

People on the ultra processed diet consumed about 500 calories more per day then was consumed on the unprocessed diet. It was observed that they also ate faster on the processed diet and gained weight. They lost weight on the unprocessed diet. On average, participants gained 2 pounds during the ultra processed diet period and lost about the same amount of weight when on the unprocessed diet.

The research team isn’t quite sure why people tended to eat more with the ultra processed foods as the tastiness of the processed and unprocessed food items were rated by the participants as the same. One thought is the way unprocessed, whole foods interact with hormones that can help suppress appetite so people tend to pay more attention to the natural cues when they are full. Another thought is that people tend to eat processed foods faster which doesn’t allow our body to register when we are full even when we have overeaten.

Processed foods have been linked to increased cancer risk and shorter life spans. Too much fat, too much sugar and too much salt have long been identified as culprits responsible for expanding waistlines and soaring obesity rates.

Calories add up over time which can lead to weight gain which can lead to serious health problems. Studies such as this help researchers understand the role of nutrition in health and can help people choose foods that are both accessible and nutritious.

Unfortunately, ultra processed foods can be hard to restrict. It takes more money and time to prepare less processed foods. Telling people to eat healthier alone might not be effective for some people without access to healthier food choices. The sheer convenience of prepackaged, processed foods has advantages in terms of convenience and shelf life which keeps people buying and consuming them. And another factor between processed and unprocessed foods is price. The foods included in the recent study were priced at about $106 per week for the ultra processed foods and $151 per week for the unprocessed foods.

The team now needs to figure out what specific aspect of the ultra processed diet affects people’s consumption behavior which led to weight gain. Their next step is to design additional studies with a reformulated ultra processed diet to see if any changes can make the diet effect on intake of calories and body weight disappear. Slight differences in protein levels between the unprocessed and ultra processed diets could possibly explain as much as ½ the difference in calorie consumption.

To view the original scientific study click below

Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake.

Good News for Night Owls

night owlA simple tweak to a night owls sleeping patterns could help with sleep/wake timings, better eating habits, improved morning performance, and a decrease in stress and depression. Night owls are people with late waking and sleep habits.

New studies conducted by the Universities of Birmingham and Surrey in the U.K. and Monash University in Australia, have shown that over a period of three weeks it was possible to shift night owls circadian rhythm. The good news is this occurred using practical and non pharmacological interventions.

Participants in the study showed they were able to bring forward their own sleep and wake timings by two hours with no negative effects on sleep duration. Additionally, they reported decreased feelings of stress and depression and also decreases in daytime sleepiness.

The research highlights the ability of simple non pharmacological interventions to phase advance those who are night owls and reduce elements of sleepiness and mental health. And they were able to manipulate peak performances in the real world.

The study included 22 healthy adults who had an average bedtime of 2:30 a.m. and a wake up time of 10:15 a.m. For the three week period, the participants were asked to wake up 2 to 3 hours before their normal wake up time and also maximize outdoor light throughout the morning. They were also asked to go to bed 2 to 3 hours before their normal bedtime and limit their light exposure during the evening. They were instructed to keep both sleep and wake times during both free and work days. They were to have breakfast as soon as possible after waking up, eat their lunch at the same time each day, and refrain from consuming dinner after 7:00 p.m.

The studies results highlighted an increase in physical (grip strength) and cognitive (reaction time) performance during morning hours when tiredness is typically high in night owls. The study also showed a shift in peak performance time from evening to afternoon. They also noted an increase in the number of days breakfast was consumed and better well being.

By engaging in simple new routines, night owls could see their body clock adjusted which leads to overall mental and physical health. Circadian misalignment and insufficient levels of sleep can disrupt many body processes putting individuals at increased risk for cancer, diabetes and cardiovascular diseases.

Night owls seem to be more compromised than morning larks due to having to fit to school and work schedules that are not in sync with their preferred patterns. The team now wants to understand how habitual sleep patterns relate to the brain, how this also links to mental well being and if interventions can lead to long term changes.

To view the original scientific study click below

Resetting the late timing of ‘night owls’ has a positive impact on mental health and performance.

Oral Health and Alzheimer’s

weightA new study conducted by researchers at the University of Bergen, Norway, have discovered a significant connection between good oral health and Alzheimer’s Disease. They determined that gingivitis has a very decisive role in whether someone develops this disease or not.

What they discovered by DNA based proof is that bacteria which cause gingivitis can actually move from the mouth to the brain. This bacteria then produces a protein that will destroy nerve cells in the brain which leads to memory loss and ultimately Alzheimer’s.

The bacteria is not what actually causes Alzheimer’s on its own. It is the presence of the bacteria that substantially raises the risk for developing this disease. Additionally this bacteria is also implicated in the more rapid progression of the disease.

However, there is good news. There are things that a person can do to slow down Alzheimer’s. Brushing and using floss is important in preventing gingivitis. If someone already has established gingivitis and they have Alzheimer’s in their family, the need is especially important for regular visits and cleanings at the dentist.

The research team examined 53 people with Alzheimer’s. They discovered the enzyme in 96% of the cases. This knowledge now gives scientists and researchers a possible new approach for studying and attacking the disease.

A new drug that will block the harmful enzymes from the bacteria has been developed. Testing of the drug should occur within the next year.

To view the original scientific study click below

Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors.

Body Parts Respond Differently Day and Night

It has been suspected that our body’s various circadian clocks are able to operate independently from our central clock located in the hypothalamus of the brain. At the University of California, Irvine, scientists have found a way to test the theory.

The study included specially bred mice for the purpose of analyzing the body’s network of internal clocks which regulate metabolism. The team figured out how to disable the entire circadian system of the lab mice then jump start their individual clocks. For the experiment, the team activated clocks located in the inside of the skin or liver.

Their results were quite surprising as no one realized the skin or liver could be directly affected by light. Even though all other body clocks were shutdown including the central brain clock, the skin and liver knew what time it was. The organs responded to changes of light as day turned into night. The organs also maintained critical functions. In the case of the liver, this organ prepared to digest food prior to mealtime and convert glucose to energy.

The liver’s circadian clock was still able to detect light presumably through signals from other organs. When the mice were then subjected to constant darkness, the liver’s clock stopped functioning.

Through this study, the team can begin deciphering metabolic pathways which control circadian rhythms, the aging process, and overall well being. In previous studies, scientists examined how circadian clocks could be rewired through factors such as diet, sleep deprivation, and exercise.

Through further studies, the scientists plan to phase in other internal clocks so they can see how different organs communicate with each other. Further experiments could reveal ways to make human internal clocks less misaligned due to modern lifestyles. Exposure to television, computers and cellphone light before bed can scramble internal clocks.

To view the original scientific study click below.

Circadian clocks: Body parts respond to day and night independently from brain, studies show

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