NEWS
HEALTH BLOG & RESEARCH
HERE ARE THE LATEST NEWS AND RESEARCH ARTICLES FROM DEMAREST CLINIC AND ITS PARTNERS.
- Demarest Clinic
- cs@demarestclinic.com
- +66 76 390 141
HERE ARE THE LATEST NEWS AND RESEARCH ARTICLES FROM DEMAREST CLINIC AND ITS PARTNERS.
William D. Johnson · July 30, 2021
William D. Johnson · July 30, 2021
Metformin, the most common drug prescribed for type II diabetes, was discovered in 1922 and first used clinically in France in 1957. It wasn’t until 1972 that it was approved in Canada, followed by the US 23 years later for the treatment of Diabetes. Over the years, millions of diabetic patients have been prescribed Metformin. Now, almost 100 years after its discovery, we have the data and understanding of all the amazing ways that Metformin can slow your ageing.
The wheels of change turn slowly in medical treatments, despite clear evidence of their effectiveness and high safety profile. The first written record of a controlled clinical trial occurred in 1747 aboard a naval ship, the HMS Salisbury. During this age of discovery, it was commonly accepted that after eight weeks at sea, ones’ mouth would begin to rot as Scurvy took hold, leading to open sores and eventual death. Scurvy killed more mariners than anything else. On the Salisbury, Dr James Lind took 12 cases and tried six different remedies. It was apparent after only six days that the two patients given citrus fruits were recovering nicely, while the other remedies were ineffective. It was almost 50 more years before the Royal Navy adopted fruit as a protocol to prevent Scurvy. After all, it was expensive.
TAME (Targeting Ageing with Metformin) 2020 was the first large-scale clinical trial where the drug was tested for its anti-ageing efficacy. The new findings helped shed light on Metformin’s apparent ability to promote healthy ageing. Although the FDA doesn’t even recognize ageing as a legitimate target for clinical trials, let alone accelerating research or development of regenerative medicines. An initiative such as TAME is inspiring and can hopefully facilitate changes within the FDA to begin addressing the core problem of ageing as a disease, rather than the chronic illness that is simply a symptom of the disease of ageing.
Some fascinating conclusions emerged from the massive amount of data collected over treating type II Diabetic patients with Metformin. Despite the fact that Diabetes shortens your life expectancy, diabetics treated with Metformin were living 15% longer than the people without Diabetes and were 30% less likely to develop cancer. Metformin reduces the incidence of almost all age-related chronic diseases, including the horrific pathologies of Alzheimer’s and early onset of dementia.
While we are well on our way to unravelling the mystery of ageing, Lopez-Otin et al. have characterized nine distinct pathways that cause ageing and are generally acknowledged by the people who study this emerging science. Metformin basically turns down the dial on all of them, reducing the speed of ageing.
We now know that Metformin has the following nine effects that are interconnected to all nine ageing pathways:
Any one of these nine effects would make considering Metformin worth it, taken together the argument becomes seriously compelling. My goal is to introduce you to information that will slow or even reverse your ageing. Stem cell therapy, given four times a year, is the absolute gold standard for Regenerative Medicine, but it remains prohibitively expensive.
Metformin, now a generic, is inexpensive and can cost as little as a few dollars a month. Talk to your Doctor, most will prescribe off label because of its high safety profile. Hopefully, the TAME trial will usher in the era when Doctors regularly prescribe Metformin for its anti-ageing characteristics rather than just an intervention for prediabetics. We don’t know yet but imagine how many years you can add to your health span with this one intervention, especially if you don’t have Diabetes.
Western medicine has done a great job extending lifespan but not health span. Treating the symptoms of age-related chronic disease rather than its cause, the disease of ageing, we are now simply sick longer. I don’t want to live a few extra decades being ill and frail. It’s not worth it. The newest science shows that we can be vital right up until our last few months of life. A healthy death occurs over a matter of months, not years. Our health span should last almost as long as our lifespan. Metformin might be the most remarkable single intervention that we have to shorten the gap between healthspan and lifespan based on cost.
Therefore, it is my first suggestion to you because it will cost you almost nothing. I take it, and like David Sinclair, the author of “Lifespan” suggests, “I don’t leave home without it”.
The only downside to Metformin is that it can reduce your regular exercise-related muscle mass gain, yet we know now your strength increases progressively. According to Dr David Sinclair (my hero), this effect can be mitigated by not taking Metformin on days you exercise. For those of us who exercise every day, there is the one week on then off method.
Sinclair surmises with the statement that it’s vanity vs longevity. For once, I don’t entirely agree with him. I think Metformin will extend your longevity and will keep you looking younger for longer. That’s not just vanity rather longevity with vanity, and it’s smart. I work out regularly, and my muscles may not bulk as they used to, pre-Metformin. However, I like the idea of being strong and lithe, and my suits fit better.
This is the first of a series of blogs that will expose you to the leading interventions available in the industry today based on cost, effectiveness and simplicity of application. They are all safe, and the data supports it.
William D. Johnson · July 30, 2021
William D. Johnson · August 19, 2021
My last blog went into detail about how Metformin extends your lifespan and reduces the risk of most age-related diseases. I talked a great deal about the biological pathways of ageing and how Metformin can benefit each. Perhaps in too much detail. Many of you may remain unconvinced. So, I enlisted the help of Dr Aysegul Coruhlu, iconic author and anti-ageing superhero, to provide a different description of the power of Metformin and its value to our vital biological function, Metabolism, and metabolic flexibility.
Metabolic flexibility refers to your body’s ability to respond to changes in metabolic demand which means your cells should be equally adept at burning fat and glucose. Mounting evidence from clinical studies suggests that metabolic flexibility is essential to maintaining cellular energy equilibrium, decreasing with age. Metformin basically regulates the use of glucose in the energy production of your cells. The more glucose we burn, the harder it is to burn fat. Another reason why diet and intermittent fasting are important as both affect your metabolic flexibility.
Metformin reduces glucose entry in the energy-producing mitochondria of your cells. It gives your cells a hunger signal that causes them to switch to fat-burning mode. Another benefit of Metformin is to reduce sugary proteins in the body. This pathology called glycosylation increases age-accelerating residues known as AGEs. AGE production is very high in Alzheimer’s, diabetes, and rapid ageing. In particular, they cause skin ageing, sagging, wrinkling and loss of elasticity. Metformin reduces all of this while making your cells younger in their energy production.
Inexpensive with a very high safety profile, 60 years of clinical evidence proves Metformin is an effortless start in your search to close the gap between healthspan and lifespan. A concept that remains primarily unaddressed in the protocols provided by traditional reactive medical treatments. Treat the cause, not the symptoms. Mind the Gap. If you want to age slower and reduce your risk for age-related disease, talk to your doctor about Metformin. It is a cheap, safe and effective means to reduce the healthspan/lifespan gap.
William D. Johnson · July 30, 2021
Journal of Gerontology · March 27, 2023
The research paper titled “Allogenic Human Mesenchymal Stem Cell Infusions for Aging Frailty” was published in the Journal of Gerontology: Medical Sciences in 2017. The study aimed to investigate the safety and efficacy of allogenic human mesenchymal stem cell (allo-hMSC) infusions in patients with aging frailty.
Aging frailty is a common condition among older adults and is characterized by a decline in physical and cognitive functions, increased susceptibility to diseases, and a higher risk of mortality. Mesenchymal stem cells have been suggested as a potential therapy for aging frailty due to their regenerative properties and ability to modulate the immune system.
The study enrolled 15 participants aged 60 to 95 years who met the criteria for aging frailty. The participants received a single intravenous infusion of allo-hMSCs. The primary outcome was safety, and the secondary outcomes were changes in physical performance, cognitive function, quality of life, and inflammation markers. The participants were followed up for six months after the infusion.
The results of the study showed that allo-hMSC infusions were safe and well-tolerated, with no serious adverse events reported during the follow-up period. The participants showed significant improvements in physical performance, as measured by the Short Physical Performance Battery and the 6-minute walk test. The study also showed improvements in cognitive function, quality of life, and inflammation markers.
The findings of this study suggest that allo-hMSC infusions may be a safe and effective therapy for aging frailty.
This study provides evidence that allo-hMSC infusions may be a promising therapy for aging frailty. The findings of this study have significant implications for the management of aging frailty and suggest a potential new approach for improving the health and quality of life of older adults.
Journal of Gerontology · March 27, 2023
Zuzanna Walter · November 9, 2021
With a focus on extending and improving the human lifespan, the medical community continues to explore potential avenues in longevity. One such development has directed increased attention to the practice of senolytics – or, the process of flushing senescent cells from the body to discard harmful proteins.
Senescent cells are malfunctioning, aged cells which can trigger inflammation and dysfunction, developed in response to disease, injury, or cancerous formations.
These cells can remain in the body, contributing to the development of many diseases and features of aging, such as heart disease, dementia, osteoporosis, and lung disease. Removing senescent cells from mice was found to alleviate insulin resistance, cell dysfunction, and ameliorate other complications in cases of kidney failure and disease.
As an emerging strategy in the anti-aging sphere, senolytics still lack a sufficient body of research. Although prior animal-based studies concluded successful results of senolytic therapy, there is no direct demonstration of success in peer-reviewed human clinical trials to date. Recently, the Mayo Clinic revealed the result of an early human study aimed at confirming the effects of decreasing senescent cells in the body as found in animal-based studies.
Conducted by a team of Mayo Clinic researchers, the Phase I trial tested a senolytic regimen comprised of the cancer drug dasatinib (Sprycel) and plant-derived quercetin in nine patients with diabetes-related chronic kidney disease (DKD). Patients given the medication combination for a total of three days, after which the treatment was stopped.
Despite being completely eliminated from the system within a few days, the drugs and their effects appeared to last. According to study authors, the key markers of senescent cell burden decreased in both adipose tissue and skin biopsied from subjects 11 days after treatment completion, as were key circulating SASP factors compared with pre-treatment levels. The results remained persistent across measures – including blood, skin, and fat tissue analysis of senescent cell abundance.
Decreasing senescent cell numbers in two human tissues brings promise of growing understanding of senolytics and credibility of animal-based senolytic study results – which may be translatable to humans. Illustrating the mechanism of action discovered in prior research, the study implicates the potential of short-term dasatinib and quercetin treatment to improve physical functioning in patients with diabetes-related chronic kidney disease.
Senolytic therapies may provide efficacious treatment opportunities for an array of age-related diseases – chronic kidney disease, cancer, and neurodegenerative disorders – which place a significant burden on the healthcare system. Current knowledge suggests that senolytics may delay, prevent, or treat Alzheimer’s and Parkinson’s disease while enhancing longevity and improving the quality of later life.
However, the field is still new. As one of the first emerging clinical trials being reported, the latest study highlights the preliminary nature of its results. Fewer than 150 subjects have been treated, knowledge of adverse effects and potential long-term health repercussions is still growing and may further influence the development of senolytic therapy. Researchers caution against implementing senolytics into the practice setting until more information is obtained from additional clinical trials. Nonetheless, the study represents the first preliminary evidence in the promising field of senolytic therapies, verifying the potential benefit of their use on the human body.
Zuzanna Walter · November 9, 2021
William D. Johnson · January 27, 2023
Demarest Clinic offers Hyperbaric Oxygen Therapy (HBOT) to treat a variety of conditions, including carbon monoxide poisoning, decompression sickness, and wound healing. It is a medical treatment that involves breathing pure oxygen inside a pressurized chamber.
HBOT works by increasing the amount of oxygen in the blood, which can help to improve the body’s ability to fight infection and promote healing. Once inside the hyperbaric chamber, the pressure is increased to 1.3 Atmosphere. This increase in pressure causes the oxygen to be dissolved into the plasma, which allows it to be carried safely to the tissues that require it the most.
One of the most well-known uses of HBOT is for the treatment of carbon monoxide poisoning. When a person is exposed to carbon monoxide, the gas binds to the hemoglobin in the blood, preventing the hemoglobin from carrying oxygen to the body’s tissues. HBOT can help to displace carbon monoxide from the hemoglobin, allowing oxygen to be transported safely to the body’s tissues.
Another common use of HBOT is for the treatment of decompression sickness, also known as “the bends”. This condition occurs when a diver ascends from the depths too quickly, causing nitrogen bubbles to form in the blood. These bubbles can cause pain, paralysis, and even death if left untreated. HBOT can help to reduce the size of the nitrogen bubbles and increase the amount of oxygen in the blood, which can help to improve the symptoms of decompression sickness. This makes HBOT at Demarest Clinic ideal for divers visiting Phuket, Thailand’s many beautiful diving spots and may experience any of the negative and potentially fatal effects that can accompany this worthwhile hobby.
HBOT has also been used in the treatment of various wound healing disorders such as diabetes, radiation injury and crush injuries. Crush injuries present as physical trauma from prolonged compression of the torso, limb(s), or other parts of the body. HBOT improves blood flow to the wound, which can help to bring more oxygen and nutrients to the area. This can help to promote the growth of new blood vessels, which can improve the healing process.
HBOT therapy is usually administered for a period of 60 to 90 minutes, and a course of treatment typically consists of 20 to 40 sessions.
If you are interested in safe Hyperbaric Oxygen Therapy in Thailand, we can help. To schedule an appointment at our Demarest Clinic or speak to a specialist about the benefits of HBOT, please contact us.
William D. Johnson · January 27, 2023
Cleveland Clinic · November 2, 2022
Few of us know what they are or exactly how they work. But many of us have heard about the healing powers of stem cells, as well as the controversy surrounding them. Stem cells are well-debated and highly complex — with promises ranging from fixing damaged knees to regenerating receding hairlines.
But what are stem cells? And, what’s all the fuss all about?
Director of the Cleveland Clinic’s Center for Regenerative Medicine and Surgery, Amy Lightner, MD, shares the differences between stem cell types, how stem cells can be used and when to be cautious of claims that might be too good to be true.
When most of us think of stem cells, we probably recall images of Dolly the cloned sheep. While it’s true that Dolly was born of stem cells, her place in science history is just one of many advancements in the field.
In fact, there are many different types of stem cells, each of which has different responsibilities and abilities. What unifies them is their ability to regenerate into new cells.
“Regenerative medicine is an emerging field that uses innovative treatments to help regenerate or heal cell function that’s lost due to aging, disease or injury,” Dr. Lightner explains. “The way we achieve this is by using stem cells in large quantities, targeted to a certain area, that the body uses to promote healing.”
Adult stem cells are the only type of stem cells that are currently approved for medical use in the United States by the U.S. Food and Drug Administration (FDA). The term “adult stem cells” is a little confusing because they’re actually found in infants, children and adults. These cells live in a variety of tissue in our bodies — including bone marrow, muscles, your brain, your intestines and more.
Think of adult stem cells as a little army of cells that can regenerate themselves into new cells to maintain and repair the tissue or muscle where they’re found. The catch with adult stem cells is that they can’t become different types of cells (for example, blood stem cells can only become new blood cells, not skin or brain cells).
Unlike adult stem cells, embryonic stem cells have many more possibilities. Harvested during an embryo’s blastocyst stage (about five or six days after an embryo has been fertilized in a lab), embryonic stem cells have the potential to become any type of cell (called pluripotent cells). For these reasons, embryonic stem cells are the type of stem cells that generate the controversy most people associate with the topic.
Researchers have discovered stem cells in amniotic fluid as well as umbilical cord blood. These stem cells have the ability to change into specialized cells. Amniotic fluid fills the sac that surrounds and protects a developing fetus in the uterus. Researchers have identified stem cells in samples of amniotic fluid drawn from pregnant women for testing or treatment — a procedure called amniocentesis.
Stem cell therapy has been around since the 1970s, when the first adult bone marrow cells were used to treat blood disease. A bone marrow transplant allows a recipient whose bone marrow cells have been damaged by chemotherapy or disease to receive healthy bone marrow stem cells from a donor.
“Those stem cells have the potential to mature within the blood system into different immune cells that recognize and fight off different types of blood cancer. And they also have the ability to heal,” says Betty Hamilton, MD, Cleveland Clinic’s Department of Hematology and Medical Oncology.
Bone marrow transplants are currently used to treat diseases including:
Dr. Hamilton and Dr. Lightner agree that we’re only just beginning to scratch the surface of stem cell therapy. In recent years, during the height of the COVID-19 pandemic, many clinical trials were underway to explore whether stem cells could be used to help treat the damaged lungs in people severely affected by the disease.
“I think ‘potential’ is the perfect word to describe stem cells,” says Dr. Hamilton. “We know they have these anti-inflammatory and regenerative properties where they can provide a significant improvement to someone suffering from a certain disease. There are so many diseases where inflammation happens, and something needs to be repaired, and so any help the immune system can get provides a lot of potential.”
Scientists are also researching whether adult stem cells can turn into pluripotent stem cells, which would allow the cells to change into any cell type without involving the use of embryonic stem cells.
Cleveland Clinic · November 2, 2022
Dr. Ayşegül Çoruhlu · July 20, 2022
Widespread pain in the muscles is today’s common disease. Although a long way to go in treatment, there is no complete solution yet. The subject of this article is to examine the biochemical mechanism of fibromyalgia and to explain its similarity with common muscle pain in covid. Once I understand the mechanism, I will explain what we can do to stop these pains with a long list.
Fibromyalgia occurs with complaints of widespread muscle pain, decrease in the pain threshold in the muscles, tension in the muscles, stiffness in the muscles. There may be accompanying complaints; such as fatigue, weakness, depression, sleep and intestinal problems. In order to explain the cause of fibromyalgic pain, I will describe a few mechanisms.
The first mechanism I will address is the serotonin deficiency mechanism. Let’s examine the effect of decreasing serotonin, which has a place in the treatment in reducing the symptoms of fibromyalgia, on pain.
It is generally defined as the happiness hormone. Mood balance is necessary for sleep and bowel movements to be smooth. The first thing we need to know; We need an amino acid called tryptophan for the production of serotonin. We get tryptophan with food. The fate of tryptophan that comes with food is to increase serotonin in the body. Increased serotonin will work as relaxed muscles, good sleep, working gut. However, in order to get tryptophan from food, it must be absorbed from the gut. Here there is a competitor to it, which blocks the absorption of tryptophan; fructose. As fructose in the intestine increases, tryptophan absorption and therefore the amount of serotonin decreases.
In today’s diet, high fructose corn syrup, HFCS, is used abundantly in processed foods. The amount of fructose in the intestine increases, especially with the consumption of floury and sugary ready-made foods. Biochemically, this fructose interacts negatively with tryptophan, the precursor of serotonin. Especially if there is a lack of good bacteria in the gut, this interaction increases, as a result, the amount of tryptophan that passes into the blood decreases. So as we eat sweet-bread to feel good, we feel worse because of the loss of tryptophan and decreased serotonin.
Let’s assume tryptophan doesn’t compete with fructose and say we don’t eat processed foods. This time we have to look at the fate of tryptophan in the liver.
Before tryptophan becomes serotonin, it has to convert to an intermediate called 5HTP. Tryptophan can only pass to the brain in this form to become Serotonin. 5HTP becomes serotonin first and we feel relaxed and good. Since melatonin is also made from serotonin, we can provide a good sleep. However, this is the ideal scenario. Another scenario comes into play in fibromyalgia: Serotonin steal syndrome; the serotonin stealing syndrome.
The other route that tryptophan will take outside of the serotonin pathway is an undesirable route, but some situations put serotonin on that path, so we call it the serotonin stealing route; its medical name is kynurenine pathway.
If tryptophan deviates from the serotonin pathway, the serotonin and its associated melatonin decrease. This unwanted pathway is provided by two enzymes in the liver. These two enzymes, which in a way degrade tryptophan, are activated if there is stress. High cortisol decreases tryptophan and thus serotonin. One of the explanations for being in a low mood when we are stressed is that this pathway is activated. Inflammatory cytokines other than cortisol activate this pathway. (These cytokines are the cause of the muscle pain in covid, which I will explain below.) If there is an inflammation in the body, such as inflammatory diseases in the intestine, increased cytokines activate this enzyme in the liver. As a result, the production of serotonin decreases. Another point is that the activity of these enzymes, which direct tryptophan to the bad pathway (the kynurenine pathway), increases with estrogen.
So far we have learned:
Now we must examine the lack of oxygen as another cause of fibromyalgia.
The explanation is as follows: The lack of oxygen in the muscles is very important because the pain in fibromyalgia is also related to the inability to produce enough energy in the muscles. The lack of oxygen in the body turns the production of oxygenated energy for energy in the muscles to the anaerobic pathway. The residue of the anaerobic pathway is lactic acid. In fibromyalgia, lactic acid accumulates in the muscles. Fatigue, weakness and pain due to lactic acid, which we call meat cut, occurs. We cannot be content with just associating oxygen with breathing. Oxygen is also decreased in anemia. The prevalence of anemia in women increases these complaints as the blood carries less oxygen due to anemia. Since this paragraph tells us the importance of transporting oxygen to the tissues with fibromyalgia, we explain that exercise is good for fibromyalgic pain; exercise increases tissue perfusion.
Let’s move on to what can be done for the treatment of fibromyalgia:
If we come to the subject of muscle pain in Covid, a situation similar to the serotonin stealing syndrome I described above occurs. According to the results of the study, the pathway of kynurenine increases in covid positive patients. In other words, this pathway is activated instead of serotonin. I wrote that two enzymes in the liver that provide this pathway are activated by cytokines. Increased Interleukins (especially IL6) and interferon in Covid stimulate these enzymes. Tryptophan goes this way, not the serotonin pathway. Serotonin deficiency manifests itself as muscle fatigue, pain and depressive mood.
In this article, although I wrote the subject under the title of fibromyalgia, the same content would have been present even if the title was depression. Therefore, those who feel depressed, chronic fatigue, weakness, malaise, sleep problems can read this article as well as those who feel muscle pain. The solutions are also similar.
Let’s finish our article with a list of foods containing tryptophan:
I wish you a year full of youth.
Dr. Ayşegül Çoruhlu · July 20, 2022
Dr. Ayşegül Çoruhlu · April 6, 2022
As we enter each new year, we promise ourselves to strive to be healthier. In this article, I will give you some suggestions that will help you stay healthy with small habit changes you can make in 2022. I will give you tips on keeping your biological age younger than your calendar age.
First, let’s find out what makes us age fast. Then let’s make suggestions to correct these negative conditions. What are the cellular causes that age us fast?
Oxygen must be able to reach each cell sufficiently and the cell must be able to use this oxygen correctly. What could be the reasons why oxygen cannot reach the cell sufficiently?
Smoking
When cigarettes are inhaled, apart from the negative effects of harmful chemicals on health, the lack of oxygen caused by cigarettes is our main concern. Breathing cigarette smoke instead of getting oxygen with each breath reduces the oxygen going to the cells. This creates an entire hypoxia, that is, a lack of oxygen, not just the lungs. You only associate smoking with lung cancer or heart disease, but the picture is bigger. Less oxygen in the breath reduces the oxygen in the microcirculation throughout the body. When looking at the thermography machine that shows the blood flow and oxygenation in the hand veins, it is seen that the circulating oxygen in the veins in your hands decreases even in a single breath. This applies to the whole body. The same thing happens with your skin. The entire skin of people who quit smoking changes in about 90 days; gray-yellow, matte, with large pores; pink-white, There is a transition to a shiny skin with small pores. Your relatives will notice this change with amazement. In fact, there are many who are faced with the question of ‘what did you do to your skin’. Of course, quitting smoking is positive for health in every way, but I wrote it in the hope that knowing that your appearance will rejuvenate rapidly will be effective in your decision to quit smoking in 2022. Because we mostly judge rejuvenation by how we look. When you look in the mirror you don’t see the condition of your lungs, but looking at your face and realizing that you look younger is very motivating. Of course, quitting smoking is positive for health in every way, but I wrote it in the hope that knowing that your appearance will rejuvenate rapidly will be effective in your decision to quit smoking in 2022. Because we mostly judge rejuvenation by how we look. When you look in the mirror you don’t see the condition of your lungs, but looking at your face and realizing that you look younger is very motivating. Of course, quitting smoking is positive for health in every way, but I wrote it in the hope that knowing that your appearance will rejuvenate rapidly will be effective in your decision to quit smoking in 2022. Because we mostly judge rejuvenation by how we look. When you look in the mirror you don’t see the condition of your lungs, but looking at your face and realizing that you look younger is very motivating.
Problems with breathing
First of all, we should put sleep apnea on this list. It’s a much more common problem than you might think. If you have noticed that your spouse stops breathing from time to time at night, I suggest you take him to a sleep laboratory. The rate at which sleep apnea ages you competes with cigarettes and even surpasses it. During apnea, your oxygen level may drop to 80 when your breathing stops, instead of the normal level of 96 and above. This is a real moment of suffocation for the body. You should not object and start wearing the devices used for apnea.
If there is a deviation in the nose, you will still have breathing problems. You should have it treated. Allergic bodies may have a stuffy nose. If you cannot identify the substances you are allergic to, you can support yourself by reducing dairy products. You can sleep by wearing nose strips on your nose.
Superficial and frequent breathing may also occur in panic attack-like situations. Pay attention to whether you are holding your breath during the day. If so, try to stay calm and take deep breaths.
Snoring also reduces your breathing. If it heals with surgery, fix it. Most uku apnea and snoring conditions are more common in overweight people. Going down to a healthy weight should also be one of your goals this year.
Being at a healthy weight is not a situation that can be detected only on the scale, as you think. The issue is where unwanted fat is stored. Although your weight seems normal, if you have visceral fat, you are not in ideal conditions. To understand whether you have visceral fat, you should check the lubrication in your waist area and abdomen. Waist circumference of 88 cm and above in women and 102 cm and above in men indicates that you have visceral fat. Aim for your goal this year to be at least 20% below these inches. For this, the first thing you will do is to delay the dinner and lighten its content. Yes, we are not weighing this year, we are measuring with a tape measure.
It is said that sugar is sweet poison. But if you say which sugar, of course, we are talking about the sugar in processed white sugar, processed flours, ready-made desserts and instant drinks. We call these foods simple carbohydrates for short. The more simple carbohydrates we eat, the faster we age. If you ask why, these foods have a high capacity to break down our body’s proteins. There is an unhealthy interaction between certain proteins in our skin, joints, brain, in short, in our entire body, and the sugar that comes from these foods. This chemical event, whose medical name is glycation, does not return once it happens. In other words, every time you eat these foods, you will see irreversible protein damage. Residues called AGE are formed that age you fast. The abbreviation of AGE, just like its name, is the cause of aging. Even the wrinkle on your skin is a projection of this condition.
Foods that cause AGE and foods that make your visceral fat and thicken your waist are in the same group. So we should add to our diet this year the goal of delaying dinner and eliminating processed carbohydrates. Even that much will go a long way towards staying young.
Moving life
The importance of exercise is repeatedly emphasized. But my purpose here is to encourage you to be a little more active. You don’t need to go to the gym, just add outdoor walks to your life.
The mismatch between the circadian internal clock and the external clock is the topic that ages you the fastest. The circadian internal clock is adjusted to the sun. Waking up with the sun, avoiding exposure to the bright light of electronics after sunset is the simplest internal clock adjustment you can make. Maybe in 2022, you can aim to reduce the long-term staring at the screens of electronics, which we missed in the past pandemic years. It is enough to look only during the day and not to look at night hours when the sun is not normally. Remember, our natural circadian 24-hour internal clock is written entirely in our genes and is adjusted to the sun. Even if you do not immediately see the negative effects on your health as you become stubborn, be sure that this situation will age you very quickly. This year, aim to start the day by touching the sunlight.
Sleep
The most important day of the circadian internal clock adjustment should start with the sun, and end the day with sufficient darkness. In order not to disrupt our melatonin hormone production, which starts at 21 o’clock, we should never look at electronics, especially during these hours. It is necessary to replace the bright lights in the house with lamps that give yellow-red light. They should not be shiny either. At 23 o’clock, we should go to sleep in our full dark room. These are essential for producing healthy melatonin. If there is light, there is no melatonin. Without melatonin, there is no health. Melatonin isn’t just about sleep. The presence of melatonin is an antioxidant. Melatonin is anti-cancer. Melatonin reduces dementia. Melatonin reduces inflammation. The best source for melatonin is our own melatonin production. The first condition for this is to sleep in a dark room after 21 o’clock with little light and at 23 o’clock.
Everyone can find a way in this regard. Yoga, meditation, breathing exercises; being in nature, having pets, hobbies, etc. you can apply whatever helps you feel good. You should know that the stress hormones we produce in every stressful situation disrupt your healing, regeneration and rejuvenation process.
We can add a lot more to the above list in order to be rejuvenated in 2022. But even that much gives you cellular life. If the year 2022 is 12 months, maybe you will age 11 months, maybe 10 months, maybe 8 months. You don’t have to age 365 days on the cellular level just because the year is 365 days. With a little attention, you can save a ton of days and put your cells in a state where they haven’t experienced those days yet.
I wish you a year full of youth.
Dr. Ayşegül Çoruhlu · April 6, 2022
Zuzanna Walter · November 11, 2021
Hyperbaric Oxygen Therapy (HBOT) may be an effective method for delaying or even reversing cellular degeneration.
Characterized by the progressive loss of physiological capacity resulting in impaired functioning and susceptibility to diseases, the biological aging process at a cellular level has two key hallmark elements: telomere length (TL) shortening and cellular senescence.
A variety of therapeutic methods aimed at reversing or slowing down this process continues to be investigated while a novel treatment shows promise – a specialized form of oxygen therapy that may be able to reverse the aforementioned biological markers of aging.
In a new small study published in the Journal of Aging, researchers present potential breakthrough findings. Per their results, hyperbaric oxygen therapy (HBOT) may be an effective method for delaying or even reversing cellular degeneration as it was shown to lengthen telomeres and decrease levels of senescent cells, potentially helping prevent age-related illnesses such as cancer, diabetes, and dementia.
Hyperbaric oxygen therapy has been used in the past for the treatment of a wide variety of health conditions, including carbon monoxide poisoning and decompression sickness. It has proven useful for scuba divers and astronauts who face hostile environmental conditions such as extreme pressure in deep ocean or outer space. A team of researchers tested whether its benefits can be extended to the biological aging process at a cellular level as well.
Led by Dr. Shai Efrati and colleagues at Tel Aviv University and Shamir Medical Center the latest study evaluated 30 healthy adults over the age of 65 who were treated with hyperbaric oxygen therapy. The team aimed to evaluate whether hyperbaric oxygen therapy affects TL and senescent cell concentrations in a normal, non-pathological aging adult population.
The study cohort received specialized oxygen therapy five days per week for a total duration of three months. As part of the treatment, participants spent 90 minutes inside of a compression chamber breathing 100% oxygen from a mask taking 5-minute breaks at regular intervals to breathe normal air.
The oxygen therapy used in this study differs from those available in clinics. Every 20 minutes participants removed their oxygen masks, prompting a quick decline to normal oxygen levels– an abrupt change which the body interprets as a sudden lack of oxygen resulting in a chain reaction.
In their findings, the researchers reported that specialized oxygen treatment improved two key markers of biological aging. After HBOT treatment, participants had significantly longer telomeres as well as a significant decrease in senescent cells revealing the possibility of aging reversal.
“For the first time in humans, we can see that we’re not only slowing decline, but the opposite — we can reverse it,” Dr. Efrati told Insider. “We see an elongation [of telomeres] of more than 20%, something that was considered impossible in humans.”
Dr. Efrati’s previous work has tested hyperbaric oxygen therapy for the treatment of cognitive issues and traumatic brain injury. Although many have been and remain skeptical of these experimental therapies, the latest findings show great promise in the field of regenerative medicine as the first evidence that human telomeres can be lengthened during clinical treatment. Further research is needed to better understand the meaning of these results for chronic illness and longevity as well as the therapies potential side effects.
“We need to see the long term effects, and to see if we can tailor the treatment for individuals to optimize the protocol,” Dr. Efrati said as he hopes to study the treatment in a larger population that includes people who are at risk of or in early stages of these diseases.
Closing in on the overall goal of treating the aging process as a preventable condition, the latest findings are a potential breakthrough for anti-aging research. However, the therapy is experimental, costly, and time-consuming; it is unlikely to reach the public soon as it requires extremely specialized equipment, resources, and a significant a time commitment. While it is promising, HBOT will not be a magical solution overriding important factors such as diet, exercise, and lifestyle habits that invariably play a role in biological aging.
Zuzanna Walter · November 11, 2021
Zuzanna Walter · November 9, 2021
According to data from the World Health Organization, the proportion of the world’s population over the age of 60 is expected to double from 11% to around 22% by the year 2050.
With an increasing aging population at hand, it is important for healthcare professionals to combat the many medical myths surrounding the biological aging process which may detrimentally affect patient longevity and well-being.
One of these perpetuated myths is that physical deterioration with age is inevitable. Although as humans age, the body naturally experiences a degree of physical deterioration, it does not have to lead to complete impairment while the process itself can be slowed down.
As the WHO explain, “Increased physical activity and improving diet can effectively tackle many of the problems frequently associated with old age.” Including reduced strength, increased body fat, hypertension, and reduced bone density, these aging complications are not pre-determined and can be mitigated to encourage healthy aging.
Prior research has found that expecting physical deterioration increases the likelihood of it occurring; a study surveyed 148 older participants about their aging and health expectations to find that expectations played an important role in the adoption of physically active lifestyles.
Older adults who expected to endure fewer age-related health complications were reported to engage in higher levels of physical activity and viewed themselves as having higher levels of physical function. Ultimately, the study’s findings revealed that a more positive outlook influenced health outcomes, such as physical function.
Levels of physical activity have proven to be an important predictor of health in older adults; managing aging-related expectations may help patients improve lifestyle choices that will assist in maintaining physical health, fitness, and function in later life.
Furthermore, another past study found that older adults with low expectations regarding aging did not believe it was important to seek medical care, heightening their risk for adverse outcomes. On the other hand, trials have also reported that individuals with a positive self-perception of the aging process lived an average of 7.5 years longer than those with more negative perceptions, highlighting the significant of outlook.
As the findings of the aforementioned trials reveal, there is a need for lifestyle interventions aimed at increasing physical activity levels in older patients that target both expectations and outlook as related to aging as well as exercise. Understanding how patient expectations relate to their health behaviors may help design appropriate interventions tailored to this demographic in particular. Furthermore, an increased awareness of the importance of aging-related expectations in older patients may help medical professionals screen and identify individuals at risk for depression or lack of engagement in healthy lifestyle behaviors.
Although it is a belief held by many patients regardless of age, the inevitability of physical deterioration and functional impairment remains a myth. With the help of strategic lifestyle interventions – including adequate physical activity, healthy dietary habits, and a positive outlook on the aging process – older individuals can help slow down the body’s natural decline and promote optimal function as they age.
Zuzanna Walter · November 9, 2021
NAD+ (Nicotinamide Adenine Dinucleotide) is an essential coenzyme found in all living cells. It is used in mitochondrial function to convert nutrients to ATP, which gives energy to all cells, regulates DNA repair, and lengthens telomeres. While enhancing Healthy cells, NAD may also cause Senescent cells (Zombie Cells) to increase SASP production. This causes unwanted side effects like chills.
Most clinics do not take this extra step which enhances full body homeostasis by removing the burden of excess senescent cells.
Also allowing a faster more efficient uptake of NAD without the unwanted side effects.
NAD+ activates DNA repair and stimulates intercellular communication. It speeds up cell regeneration and supplies energy to cells throughout the body. Combining with stem cell procedures will enhance the results and increase energy.
Exposure to toxic environments, chemicals, pollution, and diseases causes inflammation. Chronic inflammation will damage our cells and DNA. NAD+ stimulates enzymes, which prevent and reverse cellular and DNA damage.
Revitalize Your Brain and Body with NAD+ As we age, our NAD levels decline, leading to chronic fatigue and reduced brain function. But with NAD+ IV, you can turn back the clock. It provides an energy boost to your cells, rejuvenating your brain and body. Experience improved focus, memory, mood, mental clarity, and physical function.
@demarestclinic
ScienceDaily · February 22, 2021
Intravenous injection of bone marrow derived stem cells (MSCs) in patients with spinal cord injuries led to significant improvement in motor functions, researchers from Yale University and Japan report Feb. 18 in the Journal of Clinical Neurology and Neurosurgery.
For more than half of the patients, substantial improvements in key functions — such as ability to walk, or to use their hands — were observed within weeks of stem cell injection, the researchers report. No substantial side effects were reported.
The patients had sustained, non-penetrating spinal cord injuries, in many cases from falls or minor trauma, several weeks prior to implantation of the stem cells. Their symptoms involved loss of motor function and coordination, sensory loss, as well as bowel and bladder dysfunction. The stem cells were prepared from the patients’ own bone marrow, via a culture protocol that took a few weeks in a specialized cell processing center. The cells were injected intravenously in this series, with each patient serving as their own control. Results were not blinded and there were no placebo controls.
Yale scientists Jeffery D. Kocsis, professor of neurology and neuroscience, and Stephen G. Waxman, professor of neurology, neuroscience and pharmacology, were senior authors of the study, which was carried out with investigators at Sapporo Medical University in Japan. Key investigators of the Sapporo team, Osamu Honmou and Masanori Sasaki, both hold adjunct professor positions in neurology at Yale.
Kocsis and Waxman stress that additional studies will be needed to confirm the results of this preliminary, unblinded trial. They also stress that this could take years. Despite the challenges, they remain optimistic.
“Similar results with stem cells in patients with stroke increases our confidence that this approach may be clinically useful,” noted Kocsis. “This clinical study is the culmination of extensive preclinical laboratory work using MSCs between Yale and Sapporo colleagues over many years.”
“The idea that we may be able to restore function after injury to the brain and spinal cord using the patient’s own stem cells has intrigued us for years,” Waxman said. “Now we have a hint, in humans, that it may be possible.”
Yale University. (2021, February 22). Scientists repair injured spinal cord using patients’ own stem cells. ScienceDaily. Retrieved May 16, 2021 from www.sciencedaily.com/releases/2021/02/210222124524.htm.
ScienceDaily · February 22, 2021
Zuzanna Walter · November 9, 2021
One proposed cause of aging is the accumulation of epigenetic noise – or disruptions in gene expression patterns – that lead to decreased tissue function and reduced regenerative abilities. In a recent study, researchers from the Harvard Medical School (HMS) addressed the epigenetics-based theory of aging which postulates that changes in the epigenome cause cellular malfunctions and age-related diseases over time.
Their research continues to explore whether DNA methylation drives cellular change and whether restoring functionality in living organisms is possible. Results report restored vision in mice achieved by restoring aged cells in the retina to their youthful function and a reversal of vision loss in mice with a condition mimicking human glaucoma.
The proof-of-concept study represents the first successful attempt at reversing the biological clock in animals via epigenetic reprogramming. To prove this, the team of researchers examined the potential of reversing the age of cells by controlling DNA methylation.
Led by Yuancheng Lu, research fellow at Harvard Medical School, the study’s authors examined whether the regenerative capacity of young animals can be replicated in adult mice by delivering a modified three-gene combination via an adeno-associated virus (AAV) into the retinal ganglion cells of adult mice with optic nerve injury. They targeted cells within the central nervous system as it is the first part of the body affected by aging.
“Having previously found evidence for epigenetic noise as an underlying cause of aging, we wondered whether mammalian cells might retain a faithful copy of epigenetic information from earlier in life that could serve as instructions to reverse aging,”” the research team commented.
Lu and colleagues found that the treatment had multiple beneficial effects on the eye health of mice; it promoted nerve regeneration following optic nerve injury in mice with damaged optic nerves, caused a two-fold increase in the number of surviving retinal ganglion cells after injury, and increased nerve regrowth by five times. These results suggested that the modified gene combination approach was safe and could potentially be used to revolutionize the treatment of ocular degeneration as well as that of other organs affected by aging.
Following their promising findings, Lu and his team partnered with colleagues at Schepens Eye Research Institute of Massachusetts to perform two experiments: one testing whether the three-gene cocktail could restore glaucoma-related vision loss and a second one to test whether this approach could reverse vision loss associated with the regular biological aging process.
The team found that the treatment led to increased nerve cell electrical activity as well as a notable increase in visual acuity, which was measured by the animals’ ability to see moving vertical lines across a screen in a model of glaucoma. “To our knowledge, this is the first example of vision-loss reversal after glaucomatous injury has occurred; previous attempts have focused on neuroprotection delivered at an early stage to prevent further disease progression,” the authors wrote.
Similarly, the treatment had beneficial effects on the vision of elderly mice; it was able to restore vision in older mice with diminishing vision caused by normal aging. Following the treatment, the researchers found reversed patterns of DNA methylation which suggest that DNA methylation is an active agent in the aging process.
“These data indicate that mammalian tissues retain a record of youthful epigenetic information—encoded in part by DNA methylation—that can be accessed to improve tissue function and promote regeneration in vivo,” the authors concluded.
As the first findings that prove the reversal of glaucoma-induced vision loss with no associated negative side effects in the cohort, the latest results will need to be confirmed in further animal work before human trials can be initiated. Nonetheless, the success of the new approach represents a potential breakthrough in regenerative medicine and an array of possible treatment pathways for age-related health conditions.
“Our study demonstrates that it’s possible to safely reverse the age of complex tissues such as the retina and restore its youthful biological function,” said David Sinclair, PhD, co-director of the Paul F. Glenn Center for Biology of Aging Research at HMS, who is senior author of the published paper in Nature. “If affirmed through further studies, these findings could be transformative for the care of age-related vision diseases like glaucoma and to the fields of biology and medical therapeutics for disease at large,” he explained.
Zuzanna Walter · November 9, 2021
ScienceDaily · October 23, 2020
Leukemia frequently originates from the so-called leukemic stem cell, which resides in a tumor promoting and protecting niche within the bone marrow. Scientists from the Max Planck Institute of Biochemistry in Martinsried, Germany, have found a new way to make these cells vulnerable by specifically dislodging these cells from their niches.
Since blood cells have a limited lifespan, are lost during bleeding or are used up during infections, they must be replaced continuously. This supply is ensured by the so-called hematopoietic stem cells in the bone marrow. These cells can develop into any type of blood cell.
In chronic myeloid leukemia, the hematopoietic stem cell undergoes a genetic mutation by recombining chromosome 9 and 22. As a result, gene building blocks fuse that would otherwise not be in contact with each other. The incorrectly assembled chromosome is called Philadelphia chromosome and harbors the construction manual for the so-called BCR-ABL oncogene. This causes the leukemic stem cell to behave selfishly and divide at the expense of healthy blood stem cells.
A leukemic stem cell creates an environment termed the malignant niche that ensure its survival and proliferation. To remain in this tumor-promoting niche, the leukemic stem cell uses so-called integrins to attach itself to a scaffold of extracellular proteins, the so-called extracellular matrix, and to neighboring cells. In the leukemic stem cell, the activity and function of the integrins is facilitated by an intracellular protein called Kindlin.
Peter Krenn, first author of the study, explains: “The isoform Kindlin-3 is only used by blood cells. If mice harbor leukemic stem cells that lack Kindlin-3, they do not develop leukemia. Without Kindlin-3 and active integrins, the leukemic stem cells cannot attach themselves to their niche environment and are released from the bone marrow into the blood. Since they cannot home elsewhere either, they remain in the blood. There the leukemic stem cells lack the urgently needed support, which they usually receive from the niche, and die.”
The new finding that the leukemic stem cells express a protein called CTLA-4 on their surface, which is absent from healthy blood stem cells, allowed the researchers to distinguish a leukemic blood stem cell from a healthy blood stem cell. The scientists used the CTLA-4 receptor as a shuttle to deliver a Kindlin-3 destroying compound, into leukemic stem cells. Peter Krenn explains: “CTLA-4 is only briefly present on the cell surface and is then rapidly recycled back into the cell and then back to the cell surface again. This enabled us to introduce a Kindlin-3 degrading siRNA into the cell by coupling it to a CTLA-4-binding RNA sequence, which is called aptamer. The leukemic stem cell without Kindlin-3 is flushed from the bone marrow and the leukemia loses its origin and runs out of fuel.”
Peter Krenn summarizes: “In our current study we have developed a new therapeutic approach to treat chronic myeloid leukemia in mice. However, the principle of the therapy is universally valid. The inhibited Kindlin-3 production and consequent loss of integrin function prevents the cancer cells from being able to adhere and settle in tumor-promoting niches. I assume that this method will also prevent the cancer cells of other types of leukemia from settling and that these diseases could thus become much more treatable.”
Max-Planck-Gesellschaft. (2020, October 23). New therapeutic approach against leukemia. ScienceDaily. Retrieved November 16, 2020 from www.sciencedaily.com/releases/2020/10/201023123122.htm.
ScienceDaily · October 23, 2020
By Emily Sohn· October 23, 2020
https://www.nationalgeographic.com/premium/article/inflammation-ache-pain-aging
It happens to everyone. With age come discomforts: achy joints, wounds that heal more slowly, and a rising risk for cancers, heart disease, dementia, arthritis, and other illnesses. Those changes follow an uptick in inflammatory molecules over the course of a lifetime, according to a large and growing body of research. The link between age, inflammation, and disease is so well established, it has a name: inflammaging.
Now, researchers are unraveling the details of how the inflammatory process changes over the lifespan, what instigates the shift, and how it might be possible to interfere with the process. The work suggests interventions ranging from new drugs to new motivations for healthy habits like exercise that can slow the aging process, says Ron DePinho, a cancer biology and aging researcher at the University of Texas MD Anderson Cancer Center in Houston.
Research on inflammaging also illustrates the nuanced challenge of taking the reins of inflammation to sustain health later in life. Although many people fixate on the need to reduce inflammation, it is more important to sustain the appropriate amount of it as a means toward extending quality rather than quantity of life, says Judith Campisi, a cell biologist at the Buck Institute for Research on Aging, an independent research facility in Novato, Calif.
“What happens with age is you lose control of inflammation,” she says. “Even if you’re five years old, you will never heal a wound without an initial inflammatory response. It’s not always bad. It’s sometimes good.”
As people age, according to numerous studies, increasing amounts of pro-inflammatory cytokines and other inflammation-related molecules circulate in the blood alongside a rise in localized inflammation. When the shift occurs depends on the person, DePinho says, but 50 is generally when inflammation starts to increase, with a dramatic shift after 60.
That uptick tracks closely with disease trends. Beginning in the early sixties, risks rise substantially for the most common chronic diseases of aging: cancer, diabetes, heart disease and dementia, DePinho says. Starting at 65, the number of people with Alzheimer’s doubles every five years. In the U.S., 80 percent of adults over 65 have at least one chronic condition. By age 85, a third of people may have Alzheimer’s, while a third of men and one-fourth of women have had cancer. People with more inflammation in their bodies have a higher risk of disease.
Scientists have identified a dozen biological changes that correspond with age. All of those hallmarks of aging are associated with inflammation, and inflammation is considered a pillar of aging, says Luigi Ferrucci, a geriatrician and epidemiologist at the Intramural Research Program of the NIH’s National Institute on Aging in Baltimore, Maryland.
For example, as people get older, their immune cells lose their protective functions and stop doing the job of fighting off invaders, turning into what scientists call senescent cells. Other kinds of cells can also become senescent in response to stress. They cease replicating, no longer do their jobs, and start to secrete powerful inflammatory molecules that cause yet more cells to become senescent in a self-perpetuating cycle.
Meanwhile, DNA damage inside cells accumulates over time, especially at the tips of chromosomes in protective regions called telomeres, which are long stretches of bunched-up DNA. Each time a cell divides, its telomeres become shorter until they reach a critical length that is perceived by the cell as DNA damage or instability, which may induce cellular senescence.
As telomeres become damaged, they initiate a signaling process through proteins that turn certain genes on and off. Some of the genes affected support the function of mitochondria (the cell components that produce energy). As a result of the gene disruption, mitochondria become defective and leak their DNA into cells, sparking inflammation.
Scientists used to consider telomere shortening, mitochondrial damage, inflammation, and other processes as separate theories of aging that could contribute to diseases like cancer, DePinho says. Now it is clear that all of these changes are connected and that inflammation acts like a “co-conspirator” in the aging process.
As chronic inflammation sets in, it becomes harder for the immune system to perform routine tasks, like detecting and eliminating cancer cells and pathogens, which could make people more likely to develop diseases. Inflammation in the body may also activate immune cells in the brain called microglia, according to one theory, causing inflammation, weakening the blood-brain barrier, and destroying nerve cells, ultimately contributing to the development of Alzheimer’s.
This burgeoning understanding of inflammaging as a relentless circuit of steps that all exacerbate inflammation is revealing new ways to break the cycle.
Efforts to develop anti-aging interventions that target inflammation are challenging because they need to be specific to avoid causing more harm than good, Ferrucci says. Trying to tackle the chronic inflammation of aging with general anti-inflammatory drugs, for example, could make people more susceptible to disease by impairing the inflammation that our bodies need for staying healthy. “When you have an infection, if you don’t have inflammation, you’re going to die,” Ferrucci says. “Shutting down inflammation with a bomb like a corticosteroid or some monoclonal antibodies works. It’s also quite dangerous.”
One of the most promising new strategies for dealing with inflammaging is attacking senescent cells, experts say. In mice, a low-dose combination of two drugs, called Dasatinib and Quercetin, appears to be particularly effective at getting rid of these deadbeat cells and reducing inflammation in the intestines with the potential to extend lives. Clinical trials are now underway with these and other so-called senolytics to see if the same kinds of compounds might kill senescent cells and break the cycle of inflammation and disease in people too, says DePinho.
Other ongoing approaches include efforts to identify drugs that could restore telomeres, enhance mitochondrial function, and activate anti-aging genes, a strategy DePinho is working on. Some over-the-counter supplements claim to boost levels of proteins called sirtuins, which help cells respond to stresses, and a molecule called NAD+, which helps mitochondria function, among other roles, and dwindles in half from youth to middle age. Although evidence has been seriously questioned and these products have been over-hyped, DePinho says, further study may illuminate new anti-aging properties of sirtuins.
Scientists are hopeful that they are getting closer to understanding which interventions will help most, and studies in mice illustrate the tantalizing possibilities. “Tissues retain a remarkable capacity to renew themselves if you remove the underlying instigators of the aging process,” DePinho says.
Advances in immunology are lending new insights into how we can allow good inflammation to proceed while squashing the bad that can come from too much of it, Ferrucci adds. “As we discover the nuances of inflammation,” he says, “then it may be possible to find drugs that do not shut down inflammation completely.”
For now, there are simple steps people can take to address inflammaging in their own bodies, experts say, including exercise. Regular physical activity enhances DNA repair, improves mitochondrial function, activates sirtuins, and, studies show, can reduce the risk of cancer, diabetes, heart disease, and Alzheimer’s. Regular vigorous activity is best, but as little as 15 minutes a day can make a difference, DePinho says, and even leisure activities help.
Dietary choices, too, can improve the chronic inflammatory state of inflammaging, according to a variety of studies that support eating a Mediterranean-style diet with an emphasis on whole grains, produce, nuts, and fish. Eating a wide variety of vegetables may also help sustain the gut microbiome, which tends to become less resilient and contribute to rising levels of inflammation with age. Each Saturday, when Ferrucci goes to the market to shop for the week, he buys 10 different kinds of vegetables, based on this emerging evidence. “That is something that has been suggested in the literature,” he says. “And I think that’s a simple way of following that advice.”
Body fat releases cytokines that promote inflammation, DePinho adds, so using exercise and diet to control weight can have extra benefits. He also advises people to avoid or quit smoking, a habit known to increase DNA damage and drive inflammation. Finding ways to relax is another useful goal, as chronic stress has been linked to shortened telomeres, accelerated aging, and inflammatory diseases. Adequate sleep and meditation can help reduce stress, DePinho says.
Healthy habits like these are important throughout life, Ferrucci says, but they become especially important as the mechanisms that protect our cells from damage become less functional with age. That accumulating damage is a key source of inflammation. “Intervening in any possible way becomes more important as you become older,” he says.
Emily Sohn· December 27, 2023