Gut Bacteria Linked to Age Related Conditions

Gut Bacteria Linked to Age Related Conditions

Source: Frontiers.

A new study shows for the first time that gut bacteria from old mice induce age-related chronic inflammation when transplanted into young mice. Called “inflammaging,” this low-grade chronic inflammation is linked to life-limiting conditions such as stroke, dementia and cardiovasuclar disease. The research, published today in open-access journal Frontiers in Immunology, brings the hope of a potentially simple strategy to contribute to healthy ageing, as the composition of bacteria in the gut is, at least in part, controlled by diet.

“Since inflammaging is thought to contribute to many diseases associated with ageing, and we now find that the gut microbiota plays a role in this process, strategies that alter the gut microbiota composition in the elderly could reduce inflammaging and promote healthy ageing,” explains Dr Floris Fransen, who performed the research at the University Medical Center Groningen, The Netherlands. “Strategies that are known to alter gut microbiota composition include changes in diet, probiotics, and prebiotics.”

Previous research shows that the elderly tend to have a different composition of gut bacteria than younger people.

Immune responses also tend to be compromised in the elderly, resulting in inflammaging.

Knowing this, Fransen and his team set out to investigate a potential link.

The scientists transferred gut microbiota from old and young conventional mice to young germ-free mice, and analysed immune responses in their spleen, lymph nodes and tissues in the small intestine. They also analysed whole-genome gene expression in the small intestine.

All results showed an immune response to bacteria transferred from the old mice but not from the young mice.

The results suggest that an imbalance of the bacterial composition in the gut may be the cause of inflammaging in the elderly. Imbalances, or “dysbiosis” of gut bacteria results in “bad” bacteria being more dominant than “good” bacteria. An overgrowth of bad bacteria can make the lining of the gut become more permeable, allowing toxins to enter the bloodstream where they can travel around the body with various negative effects.

Dysbiosis can have serious health implications: several disorders, such as inflammatory bowel disease, obesity, diabetes, cancer, anxiety and autism are already linked to the condition.

“Our gut is inhabited by a huge number of bacteria” explains Fransen. “Moreover, there are many different kinds of bacterial species, and the bacterial species that are present can vary a lot from person to person.”


Maintaining a healthy gut microbiota is clearly important to a healthy body and healthy ageing, but why the gut microbiota is different in the elderly is not fully understood. Many people are aware of the effect a course of antibiotics can have on the digestive system for example, but as Fransen explains, it may not be down to just one thing: “It is likely a combination of factors such as reduced physical activity, changes in diet, but also as part of a natural process.”

Most, if not all, age-related diseases can be linked back to inflammaging. Despite the fact that this particular study was conducted on mice, it is clear that maintaining a healthy gut microbiota is key to a healthy lifestyle. However, more research is needed to confirm that the human body mirrors the mice in this study.

“Both in humans and mice there is a correlation between altered gut microbiota composition and inflammaging, but the link between the two remains to be proven in humans” concludes Fransen.

The article is part of the Frontiers Research Topic Immunomodulatory Functions of Nutritional Ingredients in Health and Disease.


Source: Frontiers
Publisher: Organized by
Image Source: image is in the public domain.
Original Research: Full open access research for “Aged Gut Microbiota Contributes to Systemical Inflammaging after Transfer to Germ-Free Mice” by Floris Fransen, Adriaan A. van Beek, Theo Borghuis, Sahar El Aidy, Floor Hugenholtz, Christa van der Gaast – de Jongh, Huub F. J. Savelkoul, Marien I. De Jonge, Mark V. Boekschoten, Hauke Smidt, Marijke M. Faas, and Paul de Vos in Frontiers in Immunology. Published online November 2 2017 doi:10.3389/fimmu.2017.01385

Frontiers “Gut Bacteria Linked to Age Related Conditions.” NeuroscienceNews. NeuroscienceNews, 5 November 2017.


Aged Gut Microbiota Contributes to Systemical Inflammaging after Transfer to Germ-Free Mice

Advanced age is associated with chronic low-grade inflammation, which is usually referred to as inflammaging. Elderly are also known to have an altered gut microbiota composition. However, whether inflammaging is a cause or consequence of an altered gut microbiota composition is not clear. In this study, gut microbiota from young or old conventional mice was transferred to young germ-free (GF) mice. Four weeks after gut microbiota transfer immune cell populations in spleen, Peyer’s patches, and mesenteric lymph nodes from conventionalized GF mice were analyzed by flow cytometry. In addition, whole-genome gene expression in the ileum was analyzed by microarray. Gut microbiota composition of donor and recipient mice was analyzed with 16S rDNA sequencing. Here, we show by transferring aged microbiota to young GF mice that certain bacterial species within the aged microbiota promote inflammaging. This effect was associated with lower levels of Akkermansia and higher levels of TM7 bacteria and Proteobacteria in the aged microbiota after transfer. The aged microbiota promoted inflammation in the small intestine in the GF mice and enhanced leakage of inflammatory bacterial components into the circulation was observed. Moreover, the aged microbiota promoted increased T cell activation in the systemic compartment. In conclusion, these data indicate that the gut microbiota from old mice contributes to inflammaging after transfer to young GF mice.

“Aged Gut Microbiota Contributes to Systemical Inflammaging after Transfer to Germ-Free Mice” by Floris Fransen, Adriaan A. van Beek, Theo Borghuis, Sahar El Aidy, Floor Hugenholtz, Christa van der Gaast – de Jongh, Huub F. J. Savelkoul, Marien I. De Jonge, Mark V. Boekschoten, Hauke Smidt, Marijke M. Faas, and Paul de Vos in Frontiers in Immunology. Published online November 2 2017 doi:10.3389/fimmu.2017.01385

Regeneration of our cells, brain metabolism and exercise

This is my third week at cross fit exercise training. I wanted to know how my body can regenerate.

  • The human body is an incredible machine.
  • Part of what makes it so impressive (apart from the concept of conciousness and self awareness) is its ability to regenerate itself.
  • Your outer layer of skin, the epidermis (apart from the thicker dermis beneath), replaces itself every 35 days.
  • You are given a new liver every six weeks (a human liver can regenerate itself completely even if as little as 25% remains of it).
  • Your stomach lining replaces itself every 4 days, and the stomach cells that come into contact with digesting food are replaced every 5 minutes.
  • Our entire skeletal structures are regenerated every 3 months.
  • Your entire brain replaces itself every two months.
  • And the entire human body, right down to the last atom, is replaced every 5-7 years.
  • How Your Body Rebuilds Itself In Under 365 Days

We can really influence how this renewal process take place, by the thoughts we have, the food we eat, the life style we adopt, the environment we live in, our relationships, the exercise we take. Most of these things are about the decisions we make.

FACT: Your entire body totally rebuilds itself in less than 2 years – and 98% in less than a year.

Every cell in your body eventually dies and is replaced with new cells. Everyday is a new opportunity to build a new body!

  • Your DNA renews itself every 2 months.
  • Your skin rebuilds itself in 1 month. (especially at night)
  • Your liver rebuilds itself in 6 weeks.
  • The lining in your stomach rebuilds itself in 5 days.
  • Your brain rebuilds itself in 1 year.
  • Your blood rebuilds itself in 4 months.
  • Your body builds a whole new skeleton in 3 months.

(Some research says 2 years some say 10 years*)

There is the saying that your only as old as you feel, so that’s your subjective age.

So if you always feel sick& tired as I hear people say in there frustrating moment, guess what your probably become those thoughts.

There is also the biological age. If you have been a smoker all your life, your lungs will have aged prematurely; or if your life style is very sedentary like most modern cultures,  this will have damaging effects on the body resulting in wear and tear.

There is also the belief among many religious/spiritual followers  that we are in our truest essence an eternal soul which is ageless, timeless and dimensionless.

Of course we have our chronological age which we can not change but we can change the our perception, and decisions about the other ways we behave and age.

Red blood cells live for about four months, while white blood cells live on average more than a year. Skin cells live about two or three weeks.

Colon cells have it rough: They die off after about four days. Sperm cells have a life span of only about three days, while brain cells typically last an entire lifetime (neurons in the cerebral cortex, for example, are not replaced when they die).

Muscle regeneration

Muscle regeneration is the process by which damaged skeletal, smooth or cardiac muscle undergoes biological repair and formation of new muscle in response to death (necrosis) of muscle cells. The success of the regenerative process depends upon the extent of the initial damage and many intrinsic and environmental factors. Key cellular events required for regeneration include inflammation, revascularisation and innervation, in addition to myogenesis where new muscle is formed. In mammals, new muscle formation is generally excellent for skeletal muscle but poor for cardiac muscle; however a greater capacity for regeneration of cardiac muscle is seen in fish and some anurans. These aspects of regeneration are discussed with respect to myogenic stem cells, molecular regulation, ageing and implications for human therapies, with a strong focus on skeletal muscle. Other situations of muscle damage and restoration that do not involve necrosis (e.g. sarcomere disruption and atrophy) are here not considered as regeneration.

Key Concepts:

  • Necrosis is required for muscle regeneration.
  • Inflammation is essential to remove necrotic tissue and initiate myogenesis.
  • New blood vessel formation is required after major injury of muscles.
  • Skeletal muscle has an excellent capacity for regeneration. The major source of myogenic precursor (stem) cells is still considered to be the satellite cell, although other cells lying outside the myofibre may contribute to myogenesis.
  • The source of the myogenic precursor cells (myoblasts) varies between conventional tissue regeneration and epimorphic regeneration (where mature cells dedifferentiate).
  • The microenvironment, including the extracellular matrix, affects all aspects of regeneration, for example, the muscle precursors and their capacity for new muscle formation (and fibrosis impairs myogenesis).
  • Reinnervation is essential for functional recovery of skeletal muscle.
  • Excellent myogenesis can occur in geriatric muscle, although systemic factors essential for regeneration, for example, inflammation and innervation, may be suboptimal.
  • Mammalian heart muscle has a very poor capacity for regeneration and severe damage (e.g. heart attack) results in fibrosis and impaired function.
  • In contrast, the hearts of vertebrates such as salamanders and zebrafish can regenerate; the new heart muscle is derived from the dedifferentiation and proliferation of mature cardiomyocytes. It is hoped that an understanding of mechanisms involved in these situations will present opportunities to induce regeneration of damaged human cardiac muscle.

Adult skeletal muscle is a postmitotic tissue with an enormous capacity to regenerate upon injury. This is accomplished by resident stem cells, named satellite cells, which were identified more than 50 years ago. Since their discovery, many researchers have been concentrating efforts to answer questions about their origin and role in muscle development, the way they contribute to muscle regeneration, and their potential to cell-based therapies. Satellite cells are maintained in a quiescent state and upon requirement are activated, proliferating, and fusing with other cells to form or repair myofibers. In addition, they are able to self-renew and replenish the stem pool. Every phase of satellite cell activity is highly regulated and orchestrated by many molecules and signaling pathways; the elucidation of players and mechanisms involved in satellite cell biology is of extreme importance, being the first step to expose the crucial points that could be modulated to extract the optimal response from these cells in therapeutic strategies. Here, we review the basic aspects about satellite cells biology and briefly discuss recent findings about therapeutic attempts, trying to raise questions about how basic biology could provide a solid scaffold to more successful use of these cells in clinics.

Research is currently ongoing in determining the physiological role of satellite glial cells. Current theories suggest that SGCs have a significant role in controlling the microenvironment of the sympathetic ganglia. This is based on the observation that SGCs almost completely envelop the neuron and can regulate the diffusion of molecules across the cell membrane.[2] It has been previously shown that when fluorescent protein tracers are injected into the cervical ganglion in order to bypass the circulatory system, they are not found on the neuron surface. This suggests that the SGCs can regulate the extracellular space of individual neurons.[22] Some speculate that SGCs in the autonomic ganglia have a similar role to the blood–brain barrier as a functional barrier to large molecules.[23]

SGCs role as a regulator of neuronal microenvironment is further characterized by its electrical properties which are very similar to those of astrocytes.[24] Astrocytes have a well studied and defined role in controlling the microenvironment within the brain, therefore researchers are investigating any homologous role of SGCs within the sympathetic ganglia. An established mode of controlling the microenvironment in sensory ganglia is the uptake of substances by specialized transporters which carry neurotransmitters into cells when coupled with Na+ and Cl.[25] Transporters for glutamate and gamma-Aminobutyric acid (GABA)[26] have been found in SGCs. They appear to be actively engaged in the control of the composition of the extracellular space of the ganglia. The enzyme glutamine synthetase, which catalyzes the conversion of glutamate into glutamine, is found in large amounts in SGCs.[27] Additionally, SGCs contain the glutamate related enzymes glutamate dehydrogenase and pyruvate carboxylase, and thus can supply the neurons not only with glutamine, but also with malate and lactate


Molecule[1] Type of Ganglia Method of Detection Comments
Glutamine synthetase Mouse TG IHC Catalyzes the condensation of glutamate and ammonia to form glutamine
GFAP Rat DRG, TG IHC Upregulated by nerve damage
S100 Rat DRG IHC Upregulated by nerve damage
Endothelin ETB receptor Rat, rabbit DRG IHC, autoradiography Blockers of ETs are shown to alleviate pain in animal models
Bradykinin B2 receptor Rat DRG Electrophysiology Involved in the inflammatory process
P2Y receptor Mouse TG Ca2+ imaging, IHC Contributes to nociception
ACh muscarinic receptor Rat DRG IHC, mRNA (ISH) Role not well defined in sensory ganglia
NGF trkA receptor Rat DRG Immuno-EM May play a role in response to neuronal injury
TGFα Rat DRG mRNA (ISH), IHC Stimulates neural proliferation after injury
Erythropoietin receptor Rat DRG IHC
TNF-α Mouse DRG, TG IHC Inflammatory mediator increased by nerve crush, herpes simplex activation
IL-6 Mouse TG IHC Cytokine released during inflammation, increased by UV irradiation
ERK Rat DRG IHC Involved in functions including the regulation of meiosis, and mitosis
JAK2 Rat DRG IHC Signaling protein apart of the type II cytokine receptor family
Somatostatin sst1 receptor Rat DRG IHC Somatostatin inhibits the release of many hormones and other secretory proteins
GABA transporter Rat DRG Autoradiography
Glutamate transporter Rat DRG mRNA (ISH), IHC, Autoradiography Terminates the excitatory neurotransmitter signal by removal (uptake) of glutamate
Guanylate cyclase Rat DRG, TG IHC for cGMP Second messenger that internalizes the message carried by intercellular messengers such as peptide hormones and NO
PGD synthase Chick DRG IHC Known to function as a neuromodulator as well as a trophic factor in the central nervous system


Exercise and Lactate

In animals, L-lactate is constantly produced from pyruvate via the enzyme lactate dehydrogenase (LDH) in a process of fermentation during normal metabolism and exercise. It does not increase in concentration until the rate of lactate production exceeds the rate of lactate removal, which is governed by a number of factors, including monocarboxylate transporters, concentration and isoform of LDH, and oxidative capacity of tissues. The concentration of blood lactate is usually 1–2 mmol/L at rest, but can rise to over 20 mmol/L during intense exertion[4] and as high as 25 mmol/L afterward.

During power exercises such as sprinting, when the rate of demand for energy is high, glucose is broken down and oxidized to pyruvate, and lactate is then produced from the pyruvate faster than the body can process it, causing lactate concentrations to rise. The production of lactate is beneficial because it regenerates NAD+ (pyruvate is reduced to lactate while NADH is oxidized to NAD+), which is used up in oxidation of glyceraldehyde 3-phosphate during production of pyruvate from glucose, and this ensures that energy production is maintained and exercise can continue. (During intense exercise, the respiratory chain cannot keep up with the amount of hydrogen atoms that join to form NADH, and cannot regenerate NAD+ quickly enough.)

The resulting lactate can be used in two ways:

Oxidation back to pyruvate by well-oxygenated muscle cells, heart cells, and brain cells Pyruvate is then directly used to fuel the Krebs cycle

Conversion to glucose via gluconeogenesis in the liver and release back into circulation; see Cori cycle[12] If blood glucose concentrations are high, the glucose can be used to build up the liver’s glycogen stores.

However, lactate is continually formed even at rest and during moderate exercise. Some causes of this are metabolism in red blood cells that lack mitochondria, and limitations resulting from the enzyme activity that occurs in muscle fibers having a high glycolytic capacity.

Brain metabolism and exercise

Although glucose is usually assumed to be the main energy source for living tissues, there are some indications that it is lactate, and not glucose, that is preferentially metabolized by neurons in the brain of several mammalian species (the notable ones being mice, rats, and humans).[15][16] According to the lactate-shuttle hypothesis, glial cells are responsible for transforming glucose into lactate, and for providing lactate to the neurons.[17][18] Because of this local metabolic activity of glial cells, the extracellular fluid immediately surrounding neurons strongly differs in composition from the blood or cerebro-spinal fluid, being much richer with lactate, as was found in microdialysis studies.

Some evidence suggests that lactate is important at early stages of development for brain metabolism in prenatal and early postnatal subjects, with lactate at these stages having higher concentrations in body liquids, and being utilized by the brain preferentially over glucose.[15] It was also hypothesized that lactate may exert a strong action over GABAergic networks in the developing brain, making them more inhibitory than it was previously assumed,[19] acting either through better support of metabolites,[15] or alterations in base intracellular pH levels,[20][21] or both.[22]

Studies of brain slices of mice show that beta-hydroxybutyrate, lactate, and pyruvate act as oxidative energy substrates, causing an increase in the NAD(P)H oxidation phase, that glucose was insufficient as an energy carrier during intense synaptic activity and, finally, that lactate can be an efficient energy substrate capable of sustaining and enhancing brain aerobic energy metabolism in vitro.[23] The study “provides novel data on biphasic NAD(P)H fluorescence transients, an important physiological response to neural activation that has been reproduced in many studies and that is believed to originate predominately from activity-induced concentration changes to the cellular NADH pools.

The following will age us: drugs/medications, alcohol, obesity and negative persona.

I will vow not to stop my 30-min cross fit training every morning to keep my cells from growing old.

Moving to smaller homes

move to smaller homes

Young and old want to move to a smaller house for practical reasons, mobility and changing times. With smart phones, computers and availability of travel choices, people wanted to be mobile and not be burdened by the cost of owning a large house.

In the bay area, that means mobile homes, condos, towhouse, apartment, senior assisted living, care homes and living with other family members.

A widow in Oregon, rented out the other bedrooms in her house. A grandma lives with her grandchildren. A divorce parent lives with their adult children. Many renters share a room in a house in the bay area.

An uncle bought a house and have his relatives/family members rent out each room in the house in the bay area.

What are some other ways we can cut housing costs which eat up more than a third of our paycheck?




Now that I have a teenage daughter, I have to apply the same beliefs and walk my talk

Your choice of a marriage partner starts when you choose whom to date

What does dating have to do with whom you choose to marry? Most people don’t date people whose company they don’t enjoy. If you enjoy someone’s company, it’s very likely infatuation or even love might enter the relationship. Once that happens, after an emotional tie forms, you might think religion doesn’t matter. When our emotions stifle the messages our brains try to send, we leave ourselves vulnerable to making bad decisions that can destroy our lives and those of our children.

Long before we start to date, we should consider the kind of marriage we want to have. If you have a vibrant faith or adhere strongly to a religion, it is probably an important part of who you are. You will probably want to raise your children in your faith, worship with your spouse, and maybe have devotions as a family. Your faith may determine how you want to spend your money and your time. It may determine how you expect to spend the holidays you normally celebrate. But if you are dating someone who does not share your faith, and you fall in love, your road will not be a smooth one. If you are a Christian, you would be wise to limit your dating to Christians. It will lessen your chances of marrying a man who does not share your values and beliefs. It will lessen your chances of having God’s best in your marriage. Your parents may have told you that. Your church may have told you that. But when we are young, we don’t always listen. After all, we reason, it’s just a date. I’m not going to marry him (or her).

Connie’s comments: I am gathering comments from all of you , even stories. I know in many movies, love overpowers faith, but in reality faith and love go together.

In my caregiving business, I have interviewed many couple who were together for over 50 yrs and they told me that they respect each other and love each other that divorce is not an option, even when they belong to two different churches. In most cases the other partner converts to the faith of the spouse.

Knowing the person each day and loving that person with all of his/her persona, takes many trial and error until we discover ourselves in the process. A complete person takes the challenge, applies what to be learned from a given situation and let love prevail in the end. Loving ourselves first before we can truly love another. For happiness is the sum of acceptance, love, forgiveness and positive intention.

I still choose the intricacies of being in love, finding love and even losing love, for at the end the journey one takes in the process of finding love is memory that can be savored in a lifetime.

Love begets love, faith begets faith.