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Month: June 2019

Migraines: Relief is Possible with These Healthy Habits

Migraines: Relief is Possible with These Healthy Habits

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Migraines: Relief is Possible with These Healthy Habits
Julia Dosik BS, MPH

If you are one of the over 37 million Americans that suffers from migraines, here’s some help! You may be wondering what you can do to keep these draining headaches at bay. Well, the first place to start is to understand the facts around them.

To learn about auras and the causes & triggers of migraines, check out our Migraine Headaches 101 blog post.

Natural Methods for Prevention and Relief of Migraines

Although relief is found for some migraine sufferers through OTC or prescription medications, consider more natural approaches and lifestyle changes for migraine prevention and relief. While there is unfortunately not a way to do away with migraines forever, there are healthy lifestyle habits that may help extend your time between migraine attacks.

1. Adequate Water Hydration It is extremely important to drink enough water to hydrate your body throughout the day. The most common suggestion is to drink about eight 8-ounce glasses of water per day, which is about 2 liters (or half a gallon) per day. Of course, the amount of water will increase based on daily activity level.

2. Regular Exercise Dr. Andrew D. Hershey, a headache specialist and the chair and director of the Division of Neurology at the Headache Center in Cincinnati, states that exercise helps both the body and the brain. He recommends patients with migraines exercise 4-5 times per week for 45 minutes. 1

3. Healthy Sleep Cycles If you are a migraine sufferer, it’s vital to get adequate sleep every night for prevention. Around 7-8 hours of sleep is the common recommendation, along with going to sleep around the same time each night. Also, avoid playing on your phone and/or computer right before you go to sleep as the blue light emitted from these devices can make it harder for your brain to wind down and fall asleep.

4. Well-Balanced Diet Since prolonged hunger may bring on migraines, it’s important to avoid skipping meals and to focus on a well-balanced diet consisting of fruits, nuts, vegetables, protein and good fats (i.e. avocado, cheese, eggs, extra virgin olive oil, etc.). With that being said, it is also important to avoid the specific foods or food groups that you notice trigger your migraines.

5. Stress-Reduction Techniques Techniques such as meditation, breathing exercises, taking a walk (without your phone) and being mindful of all your surroundings, journaling and anything else that brings you relief from the daily stressors of life can be advantageous for migraine prevention.

Dietary Supplements: CoQ10 and Magnesium

In addition to these lifestyle habits, regular intake of the antioxidant CoQ10 and the mineral magnesium can also contribute to migraine prevention and relief.

Not only is CoQ10 an important nutrient for energy production in the body, human studies also show that it can help make migraines shorter in duration and less severe, all without the side effects seen in prescription medications.2 If you are a premenopausal woman with migraines, there is even better news! A new 2018 study revealed that taking CoQ10 consistently for three months can lead to significantly fewer migraine attacks and when they did occur, they did not last as long and were less severe.3

Magnesium is a vital mineral that plays a role in over 300 biochemical reactions in the body. One of its major roles is relaxing smooth muscles within the blood vessels, which supports healthy blood flow in the body. When it comes to the brain, magnesium is essential in controlling brain electrical activity such as balancing excitatory-to-inhibitory actions of nerve cells as well as helping to boost blood flow. Studies show migraine sufferers are deficient in magnesium.4 For migraine prevention, magnesium oxide is one of the most frequently recommended nutrients by neurologists for their migraine patients. In fact, magnesium’s effectiveness is seen primarily in patients who have or have had aura with their migraines.5

Don’t Give Up, Don’t Give in!

Although migraine headaches come with a host of distressing symptoms, educating yourself on your triggers and avoiding them as best as you can could make a world of difference. Maintain your healthy lifestyle habits, take your nutrients daily (and medication as needed), be gentle with yourself when one does come on and take all the rest that you need! Migraines DO pass. You are NOT alone in what you are experiencing. For even more helpful migraine information, visit the Life Extension Migraine Headache Health Protocol.

About the Author: Julia Dosik, BS, MPH, is a clinical corporate trainer at Life Extension headquarters in South Florida. She holds a Bachelor of Science in biology and psychology as well as a Master of Public Health specializing in health education. Julia utilizes a mix of in-person, virtual and written training to educate employees and consumers on how the human body functions and the importance of supplementing with science-backed ingredients. It is her deepest belief that high-quality dietary supplements are fundamental to an individual’s physical and mental well-being.


  2. Shoeibi A, Olfati N, Soltani Sabi M, et al. Effectiveness of coenzyme Q10 in prophylactic treatment of migraine headache: an open-label, add-on, controlled trial. Acta Neurol Belg. 2017 Mar;117(1):103-9
  3. Dahri M, Tarighat-Esfanjani A, Asghari-Jafarabadi M, et al. Oral coenzyme Q10 supplementation in patients with migraine: Effects on clinical features and inflammatory markers. Nutr Neurosci. 2018Jan 3:1-9.
  4. Mauskop A, Varughese J. Why all migraine patients should be treated with magnesium. J Neural Transm. 2012 May;119(5):575-9.

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Evidence for Senescent Cells to Cause Aortic Aneurysms

Evidence for Senescent Cells to Cause Aortic Aneurysms

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Cells enter a senescent state in response to molecular damage, a toxic environment, reaching the Hayflick limit on replication, or to aid in wound healing, among other reasons. A senescent cell halts replication and begins to secrete a mix of inflammatory signals, growth factors, and other molecules that influence surrounding cells. This is useful and beneficial when it occurs in potentially cancerous, damaged cells, or as a part of the wound healing process. Normally these cells quickly self-destruct or are destroyed by the immune system. It is when senescent cells evade destruction and linger for the long term that the problems begin. The signals that are beneficial in the short term become destructive to tissue function and structure, additionally producing chronic inflammation and all of its accompanying problems.

In recent years, the research community has finally adopted the SENS Research Foundation view of aging in the matter of senescent cells – fifteen years late to the party, but better late than never. Meaningful progress requires more scientists and sources of funding to be involved than was the case a decade ago, so it is good that this is happening. Researchers have now demonstrated that growing numbers of senescent cells contribute to a wide range of age-related conditions, and are likely the primary cause for some of them, such as arthritis. In animal studies, selectively destroying a sizable fraction of senescent cells can extend healthy life spans, and reverse the progression of age-related diseases. Senescent cells are in effect actively maintaining a disrupted, dysfunctional state of tissue function and metabolism. Removing them turns back these consequences, producing a narrow form of rejuvenation. Aging is itself an accumulation of damage, and these senescent cells are a form of damage.

The evidence for cellular senescence to be a significant contributing cause of specific age-related conditions continues to accumulate, and ever faster as more funding pours into this part of the field. The research results noted here are an example of the type, new discoveries in the relevance of senescence to age-related disease that are announced every few months. The more that is discovered, the better for all of our futures, given that work continues on ever better ways to remove senescent cells from old tissues. That the catastrophic thinning and structural failure of aorta walls involves senescent cells is one more potential benefit to be realized by senolytic therapies capable of clearing senescent cells.

Scientists find potential way to defuse ‘time bomb’ of cardiology

Ascending aortic aneurysms grow for decades without any warning signs and can be fatal once they rupture. It is known that these aneurysms are caused by the thinning of the aortic wall which weakens it and makes it silently grow like a balloon over time without any symptoms. If caught early enough, they can be surgically repaired at low risk, but if they go undetected, which many do, they will eventually rupture or cause a tear in the wall of the aorta, called an aortic dissection. While the phenomenon is well documented, the medical community previously had little evidence to understand the mechanisms causing it to occur or how to prevent it.

Now, researchers have shown that a process that is recognized in cancer biology is causing the cells to become destructive and eat away at the surrounding muscle tissue, weakening the aortic wall. “We discovered that within the wall of the aorta, a small proportion of the muscle cells have entered into a state called senescence. Rather than die, these senescent cells become destructive, secreting enzymes that chew the area around them. There are select research groups around the world that are coming up with compounds that have shown promise in clearing out senescent cells. They are thinking about it for certain aging-related diseases, but it could be positioned for this important problem as well.”

Seno-destructive smooth muscle cells in the ascending aorta of patients with bicuspid aortic valve disease

We undertook in situ analysis of ascending aortas from 68 patients, seeking potentially damaging cellular senescence cascades. Aortas were assessed for senescence-associated-ß-galactosidase activity, p16Ink4a, and p21 expression, and double-strand DNA breaks. The senescence-associated secretory phenotype (SASP) of cultured-aged bicuspid aortic valve (BAV) aortic smooth muscle cells (SMCs) was evaluated by transcript profiling and consequences probed by combined immunofluorescence and circular polarization microscopy. The contribution of p38 MAPK signaling was assessed by immunostaining and blocking strategies.

Herein, we report that senescent SMCs accumulate in aneurysmal ascending aortas associated with bicuspid and tricuspid aortic valves. Moreover, we identified a particular predisposition to SMC senescence in BAV aortopathy, indicated by the presence of senescent SMCs in non-aneurysmal BAV aortas, enrichment of cellular senescence at the aortic convexity, and multivariable analysis of potential aneurysm risk factors. We further show that senescent aortic SMCs have a pronounced collagenolytic SASP, a destructive profile that is controlled by p38 MAPK. The findings identify a cellular aging cascade in human BAV disease and a “seno-destructive” SMC phenotype that may underlie the aortic wall degeneration.

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Can tomato juice improve your blood pressure?

Can tomato juice improve your blood pressure?

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In answer to the question of whether drinking tomato juice has a positive influence on your blood pressure level, the answer is a resounding “yes,” based in part on a recent, yearlong clinical study in Japan involving 481 men and women.

The study, published in Food Science & Nutrition, involved participants, aged between 21 and 74 years, who were supplied with as much unsalted tomato juice as they wanted (consuming an average of just under a cup of tomato juice per day) after being screened for such cardiovascular risk factors as blood pressure, glucose tolerance and their serum lipid profiles.1

At the end, new screenings revealed that 94 individuals with high and moderately high blood pressure levels, including some untreated, had significant decreases in both their systolic and diastolic blood pressure, with no other changes made in their overall lifestyles.

“Further, the serum low‐density lipoprotein cholesterol (LDL‐C) level in 125 participants with untreated dyslipidemia (high levels of fat in the blood) significantly decreased.”2

Researchers identified the antioxidant lycopene as not only the natural pigment that gives tomatoes their deep red color, but the fruit’s most abundant natural carotenoid. Cooking tomatoes, for tomato paste, for example, increases their potency and bioavailability,3 and promoting increased lycopene absorption in your gut.

Other plant-based foods contain lycopene, but not nearly as much as there is in tomatoes. Other nutrients in tomatoes include flavonoids such as rutin, kaempferol and quercetin, lutein (another carotenoid), vitamin C, folate and potassium.

All of these ingredients help maintain heart health, but increasing your potassium intake may be one of the most important changes to make in your diet to lower your cardiovascular disease risk.

Further, people who have the lowest levels of lycopene in their blood have a higher increased risk for atherosclerosis, aka acute plaque buildup, and greater arterial thickness and stiffness.4 People with atherosclerosis in their carotid arteries (leading to the brain) that can be detected by ultrasound also have lower blood levels of lycopene compared with people with normal carotids.5

Additional studies show lycopene to be associated with numerous advantages for your heart, specifically strong antioxidant activity. The luscious red fruit (not the vegetable most think it is) contains many other beneficial antioxidants, including alpha tocopherol (vitamin E), alpha carotene, beta-carotene and retinol (vitamin A), but none at nearly the level of lycopene.

Lycopene for blood pressure may improve your heart, too

An Israeli study in 2001 noted that lycopene, as found in tomatoes, is also found in other fruits and vegetables. One reason it’s an effective antioxidant is because it inactivates free radicals.6 Researchers in Finland revealed that due to the abundant provision of lycopene in tomatoes and other produce, the risk of ischemic stroke could be lowered by 59%.7

Study subjects included 1,031 middle-aged men. Those with the highest levels of lycopene in their blood were found 55% less likely to have any type of stroke compared to people with the lowest amounts. For the most common type of stroke — those caused by blood clots — men were assessed as being 59% less apt to have a stroke. According to University Health News:

“This is the first study to document a decreased stroke risk with lycopene consumption, although previous observational studies have shown that lycopene consumption is associated with lower rates of heart disease and atherosclerosis, as well as with a reduced risk of dying from any cause.

Clinical trials have also shown that lycopene benefits include lowering cholesterol, blood pressure, inflammation, and oxidative stress, including free radical damage to LDL cholesterol. Since all of these harmful processes are involved in the development of strokes, the Finnish researchers’ findings come as no surprise.”8

The implications for cardiovascular disease (CVD) and its various spin-offs are enormous. According to the World Health Organization (WHO), they’re the most common cause of mortality in the world, with 15.2 million deaths recorded in 2016 alone.9

Even if it’s not terminal, CVD can cause permanent organ damage that can lead to devastating quality of life consequences, most often due to atherosclerosis, which could be called acute plaque buildup, which eventually hardens and narrows your arteries.10

Related diseases such as diabetes and high blood pressure are contributors with their own implications; heart-related disorders weigh heavily on each other, so regulating your blood pressure, as well as your lipid and glucose metabolism, helps to prevent CVD development and its widespread complications.

Lycopene has even more ways to improve your health

There are plenty of studies showing that increasing your lycopene levels brings about several layers of cellular benefits, reducing incidences and even exerting a preventative effect on diabetes and cardiovascular disease, as well as cancer and Alzheimer’s. The journal Molecules11 notes several significant findings on lycopene, citing studies:

  • Human plasma lycopene levels have shown an inverse association with oxidative DNA damage.12
  • Previous studies have reported lycopene-rich diet and lycopene supplementation provided protective effects against DNA damage in both normal and cancerous human cells.13,14
  • Consumption of lycopene-rich foods, juices or supplements has demonstrated protective effects against DNA damage in lymphocytes.15,16,17
  • A high protection of lymphocytes from oxidative damage due to singlet oxygen and nitrogen dioxide was found in human subjects with higher intake of lycopene-rich tomato juice.18
  • Lycopene can protect human lymphoid cells from singlet oxygen by binding to the surface of the cells.19

Lycopene captures reactive oxygen species (ROS) to prevent fats, proteins and DNA strand damage, which cause aging and higher disease risks. ROS attacks your body constantly and in many ways, some we can’t do much about and some we can, from smoking to air pollution to eating primarily processed foods. One study explains how oxidation is a factor in high blood pressure, also known as hypertension:

“ROS can play, and in fact they do it, several physiological roles (i.e., cell signaling), and they are normally generated as by-products of oxygen metabolism; despite this, environmental stressors (i.e., UV, ionizing radiations, pollutants, and heavy metals) and xenobiotics (i.e., antiblastic drugs) contribute to greatly increase ROS production, therefore causing the imbalance that leads to cell and tissue damage (oxidative stress) …

If not strictly controlled, oxidative stress can be responsible for the induction of several diseases, both chronic and degenerative, as well as speeding up body aging process and cause acute pathologies (i.e., trauma and stroke).”20

Another way high lycopene levels in your body produce dramatic, health-promoting benefits has to do with its mechanisms, and studies21 specify four ways lycopene works. It:

  • Facilitates cell-to-cell communication at sites called “gap junctions,” which are crucial for cells to stop growing at the right time, which is key for preventing the development of cancer.
  • Stimulates the immune system to help destroy encroaching microorganisms and early cancer cells.
  • Regulates endocrine (glandular) communication pathways.
  • Regulates the cell reproductive cycle, preventing cancer development.

The problem with statins

Ischemic strokes, known for being clot related, take place when blood vessels in the brain become so narrow they’re more easily clogged by fatty deposits, aka plaque, which cuts off the blood flow to brain cells. When taking 25 mg of lycopene via both the diet and supplementation, patients with slightly elevated cholesterol were found to have comparable results in lowering cholesterol as that of statins.22

Statins, the most profitable drug ever sold, have grossed more than $1 trillion. It’s ironic, because additional studies show that people who take them die more often than people given placebos. Also ironic is the fact that evidence does not exist that proves lowering cholesterol or LDL does anything to improve anyone’s health.

As it happens, low cholesterol levels are a health concern. Cholesterol is found in every cell in your body, helping to produce cell membranes, hormones (including the sex hormones testosterone, progesterone and estrogen) and bile acids that help you digest fat.

What eating tomatoes can do for you

One way to demonstrate what lycopene can do for you is to show what happened when researchers extracted it from the diets of postmenopausal women for a month: Lutein and zeaxanthin, α and /β –carotene, glutathione peroxidase and superoxide dismutase were all significantly decreased in the women’s blood profiles. They concluded:

“Daily consumption of lycopene may be important as it acts as an antioxidant to decrease bone resorption in postmenopausal women and may therefore be beneficial in reducing the risk of osteoporosis.”23

One of the best things about the lycopene in tomatoes is that you can get the most benefit when it comes through foods, including tomato paste, tomato sauce, tomato soup, tomato juice and other lycopene-rich produce, like watermelon,24 a 2001 study notes. According to Edward Giovannucci, a professor of nutrition and epidemiology at the Harvard School of Public Health:

“Supplements may give you a purified form of lycopene, but you’re not sure you’re getting what you get from food. You may be getting the wrong form of lycopene in a supplement. There are also a lot of compounds in food that aren’t lycopene but that are similar, and some of those molecules may be part of what makes lycopene so beneficial.”25

  • While they may be smaller, eating organic tomatoes rather than conventionally grown provides even more phenolic benefits.26
  • When it comes to ketchup, the organic variety contains around 57% more lycopene.
  • Whether they’re raw or cooked, include a healthy fat such as olive oil when you eat tomatoes since lycopene is a fat-soluble nutrient.27
  • Heating tomatoes for 30 minutes at 190.4 degrees F (88 degrees C) — roughly the temperature at which you’d simmer soup on the stove — boosts absorbable lycopene levels.28
  • Tomatoes are in the Environmental Working Group’s Dirty Dozen,29 which lists the top 10 fruits and vegetables containing the highest levels of pesticide residue, so if you can’t buy organic or grow your own, wash tomatoes thoroughly before eating.

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Mesenchymal Stem Cells Improve Heart Regeneration via Macrophage Polarization

Mesenchymal Stem Cells Improve Heart Regeneration via Macrophage Polarization

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It is well known that the most commonly available forms of stem cell therapy produce benefits via signaling on the part of the transplanted cells, which soon die, rather than via any sort of integration of these cells into tissues. These treatments use varieties of what are called mesenchymal stem cells, which is actually a poorly defined, broad category. One clinic’s mesenchymal stem cells are usually meaningfully different from those of the next. Nonetheless, these therapies fairly reliably reduce chronic inflammation. This can allow for improved regeneration in patients, but that outcome is much less reliable in practice.

The innate immune cells known as macrophages are important in the complex dance of tissue regeneration. In recent years researchers have become increasingly interested in deciphering and altering macrophage behavior, switching more of these cells from the aggressive and inflammatory M1 polarization, responsible for hunting pathogens, to the pro-regenerative M2 polarization. It is thought that aging is characterized by too much of a bias towards M1, and the balance might be forced back to M2 via the application of suitable therapies. It is perhaps not surprising that we should find that some existing therapies that can modulate inflammation and improve regeneration act through this mechanism.

Myocardial infarction (MI) is a major cause of coronary heart disease (CHD). More and more studies have shown that stem cells can play an important role in tissue repair and anti-inflammation. In particular, mesenchymal stem cells (MSCs) have shown anti-inflammatory and immunological functions. Indeed, MSCs have also been shown to have the potential to enhance the recovery and regeneration of the infarcted myocardium. The current belief on the role of MSCs in myocardial regeneration is their synthesis and secretion of cytokines and other trophic growth factors to signal to the injured myocardial cells, which may also involve anti-aging effects.

We have recently shown that the effects of transplantation of CD146+ MSCs on myocardial regeneration after MI exceeds the effects of transplantation of MSCs, likely resulting from reduction of aging-associated cellular reactive oxygen species in injured cardiac muscle cells (CMCs). Many effects of MSCs on tissue repair and cell regeneration are conducted through their crosstalk with macrophages. It is traditionally thought that macrophage are deemed to be white blood cells with a major functionality of swallowing and ingesting wastes, dying or dead cells, and impurities. Nevertheless, recently studies have shown that macrophages have much more functions other than phagocytosis. Therefore, a more complicated classification of macrophages has been applied, in which 2 subtypes of macrophages are distinguished by two phenotypes. One was named as “M1” macrophages, while the other alternatively polarized one was named as “M2” macrophages, which function in regulation of humoral immunity and promotion of tissue repair.

Since the role of macrophages in the MSC-mediated recovery of heart function after MI remains unclear, this question was thus addressed in the current study. We found that transplantation of MSCs did not alter the total number of the macrophages in the injured heart, but induced their polarization towards a M2-phenotype. Moreover, administration of TNFα into MSC-transplanted mice, which prevented M2-polarization of macrophages, abolished the effects of MSCs on recovery of heart function and on the reduction of infarcted cardiac tissue. Thus, our data suggest that MSCs may rejuvenate CMCs after ischemic injury at least partially through induction of M2-polarization of macrophages.


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The Goal of Kidney Rejuvenation

The Goal of Kidney Rejuvenation

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The authors of this open access paper review the aging of the kidney and consider the prospects for using factors from young blood as a means of rejuvenation. This is a fairly narrow view, as there are many other approaches that should produce rejuvenation of the aged kidney, ranging from those close to realization, such as senolytic therapies to clear senescent cells, or various approaches to stem cell therapy, to those yet to be achieved, meaning much of the rest of the SENS agenda of rejuvenation biotechnologies to repair the damage that causes aging. Nonetheless, after so many years of trying to persuade the research community to open up on the topic of addressing the mechanisms of aging as a means of therapy, it is very pleasant to see so many publications in the literature doing just that. The present open discourse is a sea change in comparison to the silence of a decade or two ago, in which few researchers were willing to speak in public about treating aging. The science was always valid and promising, it is the culture that has changed for the better.

It is well established that aging is associated with structural and functional renal changes. With the possible exception of the lung, the changes in kidney function with normal aging are the most dramatic of any human organ or organ system. The normal kidney loses about 25% of its mass during aging, with the loss involving both cortical glomeruli and tubules. Functionally, the aging kidney has a parallel decline in both glomerular and tubular function. The Baltimore longitudinal study demonstrated an average of 0.75 mL/min/year decline in glomerular filtration rate (GFR) in 254 men without hypertension or kidney disease. The GFR loss rate is tripled in subjects over 40 as compared with those under 40.

Cellular senescence describes an everlasting growth arrest of still viable and metabolically active cells. The cell-cycle regulators and tumor suppressors p16Ink4a and p19ARF are involved in cellular senescence. The expression of p16 Ink4a in the kidney has been known to increase with age and could be found in a variety of renal cell types. Renal p16Ink4a expression has been suggested as an ideal marker for renal aging and shown to foresee transplant outcome. In normal human glomerular, p16Ink4a expression is increased with age and in all resident cell types. Studies in a transgenic mouse model confirmed that ablating p16Ink4a positive senescent cells not only prolongs the lifespan, but also attenuates glomerulosclerosis in aging kidney and decreasse blood urea nitrogen levels. Furthermore, depletion of p16Ink4a resulted in reduction of renal interstitial fibrosis and nephron atrophy in mice after ischemia-reperfusion injury, indicating inhibition of senescence provides a protective effect on the development of fibrosis.

Considering the increase of the aging population, it is extremely urgent to identify a way to retard the aging process or rejuvenate the community. To test the effects of young blood on aged organ, young blood infusion or parabiosis may be used. Parabiosis is an experimental model aiming to join the circulatory system of two animals. Heterochronic parabiosis is used to connect an aged partner to a young partner, and can be used to demonstrate the effects of young blood on aged organs, and vice versa. With this model, rejuvenation in the aged heterochronic parabiont has been shown in different organs such as muscle, liver, brain, and heart.

In aged kidneys, a recent study showed that young blood environment enhances the autophagy of aged kidney through down-regulation of aging-related protein p16Ink4a and SA-β-gal, up-regulation of autophagy factors Atg5 and LC3BII, and down-regulation of autophagic degradation protein p62. Moreover, recent studies provided evidence that young systemic milieu may alleviate renal ischemia-reperfusion injury in elderly mice probably through reduction of oxidative stress, inflammation, apoptosis, and enhancement of autophagy in the injured aged kidney. Although evidence showed that young blood can attenuate renal aging and injury induced by ischemia-reperfusion injury in elderly mice, it will be important to identify and study the effects of specific blood-borne rejuvenating factors in the young blood or aging factors in the old blood in addition to put efforts into delineate the mechanisms underlying the renal cell senescence. This information will provide novel ideas to turn back the clock of the aging kidneys.


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The Urge to Radical Life Extension

The Urge to Radical Life Extension

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Those portions of the modern longevity community interested in bringing an end to aging and extending healthy human life span indefinitely tend to be the older portions, people who have been a part of the broader movement for quite some time. Newcomers tend to be more moderate, aiming at lesser goals. Perhaps this is a result of the successful projects, such as the SENS Research Foundation and Methuselah Foundation, tending to moderate their rhetoric as they attract a broader and larger base of support. I think that this road to moderation might be a problem, and that there is thus a continued role for those who loudly declaim that the goal is to control aging absolutely, via new medical technology, and that the natural consequence of that control is healthy, active, youthful life that extends for centuries or more.

If the goals that our movement works towards are broadly watered down from radical life extension of centuries to just adding a few more years, then marginal projects that can do no more than add a few more years will come to dominate the field to the exclusion of everything else. We are already more or less in this situation, in that that the vast majority of funding goes towards discovery and development of small molecules that tinker with the operation of an aged metabolism to make it a little more resilient to the underlying causes of aging. If that is all that is done, then we’ll all age and die on basically the same schedule as our parents and grandparents. It will be a grand waste of opportunity, given that we have the knowledge and the means to do far better, such as by following the SENS agenda for rejuvenation biotechnologies based on repairing the root causes of aging.

This popular media article looks at a few of the people who do make no bones about aiming at radical life extension. It isn’t terrible, thankfully, though it doesn’t quite manage to escape the straitjacket of conformity, the author suggesting that it is somehow strange to want to live for a long time in good health, or strange to want to avoid a slow, crumbling, painful death. There is no present status quo so terrible that it will not have its defenders, and for whatever reason the status quo of aging and suffering and omnipresent death and loss are aggressively defended. But setting that aside, the article manages to capture the present state of development and the viewpoints of its subjects quite well, which is a change over past years of media attention.

How to live forever: meet the extreme life-extensionists

In 2016, an American real-estate investor named James Strole established the Coalition for Radical Life Extension, a nonprofit based in Arizona which aims to galvanise mainstream support for science that might one day significantly prolong human life. Standards in modern medicine are allowing us to live longer now than ever before. But that is not Strole’s concern. What good are a few more measly years? He is interested in extending life not by days and weeks, but by decades and even centuries, to the degree that mortality becomes optional – an end to The End. He isn’t alone. Life extensionists have become a fervent and increasingly vocal bunch. Famously, the community includes venture capitalists and Silicon Valley billionaires, non-gerontologists all, and nearly all men, who consider death undesirable.

The current life-extensionist strategy is twofold. First, achieve a “wellness foundation,” Strole says. Second, stay alive until the coming gerontological breakthrough. All that is required is to “live long enough for the next innovation,” and presuming you do, “You can buy another 20 years.” Twenty years here, 20 years there, it all adds up, and suddenly you’re 300. This is a common view. Last year the British billionaire Jim Mellon, who has written a book on longevity, titled Juvenescence, said: “If you can stay alive for another 10 to 20 years, if you aren’t yet over 75 and if you remain in reasonable health for your age, you have an excellent chance of living to more than 110.” To most, 110 seems a modest target. Why not forever? “It’s not some big quantum leap,” Strole says, by way of explanation. He invokes the analogy of a ladder: “step by step by step” to unlimited life. In 2009 the American futurist Ray Kurzweil coined a similar metaphor, referring instead to “bridges to immortality“.

Aubrey de Grey, a serious scientist, considers life extension a health issue, which is perhaps the field’s most convincing argument. Gerontologists are not hoping to end death, he says. Instead, “We’re interested in people not getting sick when they get old.” No matter how much society rails against the concept of immortality, nobody really wants to suffer through Alzheimer’s, or suddenly fall foul of cardiovascular disease. Gerontology is the act of developing treatments for age-related diseases, de Grey argues – of reducing the causes of death, not death itself. “The benefits of living longer are not the point. The benefits are not having Alzheimer’s disease.” For de Grey, indefinite life is a by-product, not a goal.

Are we anywhere near to a breakthrough? So far, research has produced modest yields. Gerontologists speak prophetically of potential, but most warn a significant human development remains somewhere far off in the distance – almost in sight but not quite. Richard Hodes, the director of the National Institute of Aging, a US government agency, told me that, though research in animals has led to “dramatic increases in lifespan”, some of them multi-fold, “There has been far less quantitative effect as those models have moved towards mammalian species.” The biologist Laura Deming, who in 2011 established the Longevity Fund, a venture capital firm that supports “high-potential longevity companies”, told me that startups continue to successfully root out biological markers of ageing – inefficient cells, mitochondrial decline – but that, in humans, “We really don’t know right now what will work and what won’t.”

Much of gerontology focuses on identifying types of damage that accumulate with age and developing ways to halt or reverse that accumulation. It has been discovered, for example, that as we grow older, certain cells become senescent and harmful but nevertheless stick around, getting in the way like comatose guests at the end of a house party. Removing those cells have helped mice have longer, healthier lifespans. Similar forms of genetic engineering have been successful in other animal models. But to reach the mainstream, gerontologists must convince government agencies to support human adoption, a complicated and long-winded task, given the general view that death is a normal human process.

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Efficiently Reprogramming Fibroblasts into Cardiomyocytes for Heart Regeneration

Efficiently Reprogramming Fibroblasts into Cardiomyocytes for Heart Regeneration

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The heart regenerates only very poorly, and responds to injury by producing scar tissue, a process that involves fibroblast cells. Additionally, the age-related disruption of regenerative processes produced by senescent cells and chronic inflammation tends to empower fibroblasts to produce fibrosis in the heart even in the absence of injury. One potential approach to the challenge of poor heart regeneration and growing fibrosis is to reprogram the fibroblasts of scar tissue into functional heart muscle cells, cardiomyocytes. Given recent demonstrations of in situ cell reprogramming, it is plausible to think that this can be accomplished. The challenge is to do so without disrupting the vital structural and electrical properties of heart tissue.

A heart attack leaves damaged scar tissue on the heart and limits its ability to beat efficiently. But what if scientists could reprogram scar tissue cells called fibroblasts into healthy heart muscle cells called cardiomyocytes? Researchers have made great strides on this front with lab experiments and research in mice, but human cardiac reprogramming has remained a great challenge. Now, for the first time, researchers have developed a stable, reproducible, minimalistic platform to reprogram human fibroblast cells into cardiomyocytes.

The researchers introduced a cocktail of three genes – Mef2c, Gata4, and Tbx5 – to human cardiac fibroblast cells with a specific optimized dose. To increase efficiency, they performed a screen of supplementary factors and identified MIR-133, a small RNA molecule that when added to the three-gene cocktail – and with further in-culture modifications – reprogrammed human cardiac fibroblast cells into cardiomyocytes at an efficiency rate of 40 to 60 percent.

Analysis identified a critical point during the reprogramming process when a cell has to “decide” between progressing into a cardiomyocyte or regressing to their previous fibroblast cell fate. Once that process begins, a suite of signaling molecules and proteins launch the cells onto different molecular routes that dictate their cell type development. The researchers also created a unique cell fate index to quantitatively assess the progress of reprogramming. Using this index, they determined that human cardiac reprogramming progresses at a much slower pace than that of the previously well-described mouse reprogramming, revealing key differences across species and reprogramming conditions.


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Amyloid-β Causes Pericyte Dysfunction and Reduced Blood Flow in the Aging Brain

Amyloid-β Causes Pericyte Dysfunction and Reduced Blood Flow in the Aging Brain

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The brain is an energy-hungry organ, and the supply of oxygen and nutrients to brain tissue is vital to its function. This is one of the reasons why cardiovascular disease contributes to neurodegeneration. Researchers know that cells that wrap small blood vessels in the brain, called pericytes, tend to become dysfunctional or die in later life, another of the cellular casualties of the damage of aging. This causes greater constriction of the blood vessels, reducing the blood flow to tissues. Researchers here provide evidence for this to be a consequence of the aggregation of amyloid-β, characteristic of the early stages of Alzheimer’s disease. This is an intriguing addition to what is known of the issues caused by protein aggregation in neurodegenerative conditions.

A new study looked at the role of pericytes, cells wrapped around capillaries that have the ability to contract and regulate blood flow. Researchers examined capillaries in Alzheimer’s-affected human brain tissue and in mice bred to develop Alzheimer’s pathology, and found that they were squeezed by pericytes. They also applied amyloid beta protein (which accumulates in the brains of people with Alzheimer’s) to slices of healthy brain tissue, and found that the capillaries were squeezed as a result. They calculated that the constriction was severe enough to halve blood flow, which is comparable to the decrease in blood flow found in parts of the brain affected by Alzheimer’s.

“Our study has, for the first time, identified the underlying mechanism behind the reduction of brain blood flow in Alzheimer’s disease. Since reduced blood flow is the first clinically detectable sign of Alzheimer’s, our research generates new leads for possible treatments in the early phase of the disease. Damage to synapses and neurons in Alzheimer’s is usually attributed to the actions of amyloid and tau proteins accumulating in the brain. Our research raises the question of what fraction of the damage is a consequence of the decrease in energy supply that amyloid produces by constricting the brain’s finer blood vessels. In clinical trials, drugs that clear amyloid beta from the brain have not succeeded in slowing mental decline at a relatively late phase of the disease. We now have a new avenue for therapies intervening at an earlier stage.”


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Migraine Headaches 101: Causes and Triggers

Migraine Headaches 101: Causes and Triggers

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Migraine Headaches 101: Causes and Triggers
Julia Dosik BS, MPH

What is a Migraine?

A migraine is a type of headache characterized by an extreme sensitivity to light, sound and/or smell, painful throbbing on one or both sides of the head, nausea, vomiting, dizziness, lightheadedness, blurry vision and an overall feeling of weakness. Do any of these symptoms sound familiar to you? If so, you could be one of the over 37 million Americans that suffer from migraines.

You may be wondering what you can do to keep these draining headaches at bay. Well, the first place to start is to understand the facts around them. What causes migraines? Is there a genetic component? What are auras? We will answer these questions below!

Migraine Causes

Although science has yet to uncover the cause of migraines, several theories have been developed. One theory is that blood flow in specific brain regions begins to decrease, which may contribute to the onset of pain localized in one area of the head. Another theory is that pain occurs due to waves of activity from excitable brain cells. These waves of activity spark chemicals in the brain to narrow blood vessels. Abnormalities in the communication between brain chemicals and nerve cells may also cause migraine episodes. For women specifically, migraines occur more often than men because of their fluctuating estrogen levels during fertile and post-menopausal years.2 However, that does not mean that men are immune to the attacks of migraines.

Do Genetics Play a Role in Migraine Headaches?

As with many other health conditions, migraines do have a genetic component. In fact, when one or both parents suffer from migraines, their children have a 50-75% chance of getting them, too.3

What are Auras?

Migraines are usually associated with visual, sensory or motor disturbances. In the context of migraines, these symptoms or sensations are known as auras. Common examples of auras include: seeing flashes of bright light, squiggly lines, blind spots in vision, tingling in the face and hands, muscle weakness and speech or language difficulty.4 In fact, some people can detect when they are getting a migraine because the aura usually precedes the pain. On the other hand, there are people that may get the aura, but do not get pain. Either way, getting an aura could actually be beneficial because it gives you time to prepare for what may come. Whether it’s taking medication or quickly getting to a dark, non-stimulating room, acting fast when experiencing an aura could save you from hours of agonizing discomfort.

Migraine Triggers

As you get to know your body more, you may find that certain foods, drinks, environmental conditions and stress can exacerbate existing conditions such as acid reflux, for example. Well, the same goes for migraines. There are certain triggers than can contribute to the onset of migraines in some individuals, especially those experiencing chronic migraines (occurring more than 15 days out of the month). Common migraine triggers are salty and processed foods, not eating and drinking enough water throughout the day, unusually bright lights, strong smells, loud noises, extreme exercise, sleep cycle changes, weather changes and even drinking too much caffeine.

You may be thinking, “but Excedrin has caffeine in it, and I take it for my migraines.” Yes, Excedrin is a popular over-the-counter (OTC) migraine medication and it does contain about 65 mg of caffeine. However, caffeine should be consumed in moderation as too much of it may lead to over overstimulation of nerve cells, which is one of the above theories behind migraine pain. The good news is that relief is possible with healthy habits and supplementation. Tomorrow, we will discuss how to get relief in part 2 of our migraine blog series.

About the Author: Julia Dosik, BS, MPH, is a clinical corporate trainer at Life Extension headquarters in South Florida. She holds a Bachelor of Science in biology and psychology as well as a Master of Public Health specializing in health education. Julia utilizes a mix of in-person, virtual and written training to educate employees and consumers on how the human body functions and the importance of supplementing with science-backed ingredients. It is her deepest belief that high-quality dietary supplements are fundamental to an individual’s physical and mental well-being.



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Mir-294 Awakens an Embryonic Proliferation Behavior in Heart Cells, Spurring Regeneration Following Heart Attack

Mir-294 Awakens an Embryonic Proliferation Behavior in Heart Cells, Spurring Regeneration Following Heart Attack

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That microRNA-294 (mir-294) beneficially affects heart regeneration was discovered via its presence in embryonic stem cell exosomes. Exosomes are extracellular vesicles, membrane-bound packages of molecules that cells pass between one another. They are interesting to the research community because it is in principle much easier to construct a therapy based on delivery of exosomes harvested from stem cells than it is to deliver those same stem cells. Thus most of the present generation of stem cell therapies may well be replaced in the near future by the delivery of extracellular vesicles, and many research groups are testing exosomes from stem cells to see how well they work to spur greater regeneration.

Most vesicles contain a wide variety of molecules, but in the case of embryonic stem cell exosomes and the injured heart, researchers found that near all of the therapeutic effect was mediated by mir-294. Thus they could go a step further and discard the exosomes as well as the cells. The results of that line of work are noted in today’s publicity materials and paper. Applying mir-294 causes adult heart muscle cells to regress into a state more like that of embryonic cells, provoking greater replication and thus greater regeneration. This sort of in-situ reprogramming of cell behavior is growing in popularity in the research community, see the work of for example, though it remains to be seen whether or not it can be made safe enough to be the basis for a near future regenerative therapies.

Embryonic MicroRNA Fuels Heart Cell Regeneration, Temple Researchers Show

By adulthood, the heart is no longer able to replenish injured or diseased cells. As a result, heart disease or an event like a heart attack can be disastrous, leading to massive cell death and permanent declines in function. A new study is the first to show that a very small RNA molecule known as miR-294, when introduced into heart cells, can reactivate heart cell proliferation and improve heart function in mice that have suffered the equivalent of a heart attack in humans. “In previous work, we discovered that miR-294 actively regulates the cell cycle in the developing heart. But shortly after birth miR-294 is no longer expressed. The heart is very proliferative when miR-294 is expressed in early life. We wanted to see if reintroducing it into adult heart cells would turn them back to an embryonic-like state, allowing them to make new heart cells.”

The researchers tested their idea in mice that had myocardial infarction (heart attack). Mice were treated with miR-294 continuously for two weeks after sustaining myocardial injury. Two months following treatment, the researchers observed noticeable improvements in heart function and a decrease in the area of damaged tissue. Examination of treated heart cells revealed evidence of cell cycle reentry, indicating that the cells had been reactivated, regaining the ability to produce new cells. “The miR-294 treatment reawakened an embryonic signaling program in the adult heart cells. Because of this, the old heart cells were no longer quite like adult cells, but neither were they fully embryonic. In this in-between state, however, they had the ability to make new cells.”

Transient Introduction of miR-294 in the Heart Promotes Cardiomyocyte Cell Cycle Reentry After Injury

Embryonic heart is characterized of rapidly dividing cardiomyocytes required to build a working myocardium. Cardiomyocytes retain some proliferative capacity in the neonates but lose it in adulthood. Consequently, a number of signaling hubs including microRNAs are altered during cardiac development that adversely impacts regenerative potential of cardiac tissue. Embryonic stem cell cycle miRs are a class of microRNAs exclusively expressed during developmental stages; however, their effect on cardiomyocyte proliferation and heart function in adult myocardium has not been studied previously.

In this study, we determine whether transient reintroduction of embryonic stem cell cycle miR-294 promotes cardiomyocyte cell cycle reentry enhancing cardiac repair after myocardial injury. A doxycycline-inducible AAV9-miR-294 vector was delivered to mice for activating miR-294 in myocytes for 14 days continuously after myocardial infarction. miR-294-treated mice significantly improved left ventricular functions together with decreased infarct size and apoptosis 8 weeks after MI. Myocyte cell cycle reentry increased in miR-294 hearts parallel to increased small myocyte number in the heart. Isolated adult myocytes from miR-294 hearts showed upregulation of cell cycle markers and miR-294 targets 8 weeks after MI. Thus ectopic transient expression of miR-294 recapitulates developmental signaling and phenotype in cardiomyocytes promoting cell cycle reentry that leads to augmented cardiac function in mice after myocardial infarction.

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