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Month: June 2019

Higher Protein Intake Correlates with Lower Risk of Frailty in Old Age

Higher Protein Intake Correlates with Lower Risk of Frailty in Old Age

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Physical weakness is a sizable component of age-related frailty. The loss of muscle mass and strength that accompanies aging, known as sarcopenia, has many potential contributing causes, with varying degrees of accompanying evidence. One of these is dietary, a lower protein intake in older individuals, and dysfunction in processing of amino acids such as leucine. That this correlates with frailty, as illustrated here, doesn’t necessarily mean that it is an important cause, however. The alternative is that the factors that lead to reduced dietary intake in later life are distinct issues that arise from similar root causes to those of sarcopenia: consider something as simple as increased difficulty when swallowing, for example. When it comes to mechanisms, there is better evidence for chronic inflammation produced by cellular senescence or declining stem cell function to be primary causes in sarcopenia, and these are not particularly related to dietary protein intake.

Frailty can be defined as a state of augmented sensitivity and vulnerability to external stressors in old age. The Fried frailty phenotype classifies frailty as the presence of three or more of the following five components: weakness, slowness, low physical activity, exhaustion, and weight loss, and prefrailty as the presence of one or two of the Fried phenotype criteria. In a recent systematic review carried out in 61,500 individuals aged 65 and older, the overall prevalence of frailty was estimated to be 10.7%, and 41.6% were prefrail with one or two components of Fried frailty phenotype.

There is growing support for the concept that greater protein intake may preserve physical function in older adults. The anabolic response to amino acid intake may be blunted in older people, particularly if they have low intakes of protein. In addition, animal protein intake may be associated with muscle strength in older adults, which may be associated with a lower risk of frailty; whereas, plant-based protein sources may have limited potential to stimulate the skeletal muscle anabolic response. The exact reasons are not understood but it might be that plant proteins are considered to have a lower content of essential amino acids compared to animal protein sources. Nevertheless, knowledge regarding the association between adequate protein intakes, according to recommendations, and sources of protein intake with frailty are limited.

We hypothesized that the prevalence of frailty and prefrailty was lower among older women consuming ≥ 1.1 protein/kg body weight (BW) compared to those with lower intakes. Participants were 440 women aged 65─72 years enrolled in the Osteoporosis Risk Factor and Prevention-Fracture Prevention Study. Protein intake g/kg BW and g/d was calculated using a 3-day food record at baseline. At the 3-year follow-up, frailty phenotype was defined as the presence of three or more, and prefrailty as the presence of one or two, of the Fried criteria. At the 3-year follow-up, 36 women were frail and 206 women were prefrail. Higher protein intake ≥ 1.1 g/kg BW was associated with a lower likelihood of prefrailty (odds ratio = 0.45) and frailty (odds ratio = 0.09) when compared to protein intake of less than 1.1 g/kg BW at the 3-year follow-up. Women in the higher tertile of animal protein intake, but not plant protein, had a lower prevalence of frailty. Thus protein intake ≥ 1.1 g/kg BW and higher intake of animal protein may be beneficial to prevent the onset of frailty in older women.


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Mitochondrial Oxidative Stress in Neurodegenerative Disease

Mitochondrial Oxidative Stress in Neurodegenerative Disease

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Aging is characterized by increasing dysfunction in mitochondria, the power plants of the cell, responsible for packaging chemical energy store molecules, ATP, to power cellular operations. Mitochondrial decline in aging is most studied in energy hungry tissues such as the muscles and brain, and it is widely accepted that mitochondrial dysfunction is an important feature of neurodegenerative diseases. Mitochondrial dysfunction is likely caused by damage to mitochondrial DNA and loss of quality control mechanisms responsible for destroying malfunctioning mitochondria. It manifests as a reduced supply of ATP and increased generation of oxidative molecules.

Oxidative reactions that disrupt cellular machinery occur constantly even in youth, and cells possess many antioxidant and repair mechanisms to keep this damage under control. Oxidative damage is even used as necessary signaling in processes such as the beneficial response to exercise. Consistently raised amounts of oxidative molecules are harmful in many ways, however, not just damaging internal cellular operations, but also producing downstream issues such as altered forms of cholesterol that contribute to the progression of atherosclerosis.

Aging is the primary risk factor for a number of human diseases, as well as neurodegenerative disorders. A growing body of evidence highlights bioenergetic impairments as well as alterations in the reduction-oxidation (redox) homeostasis in the brain with the increasing of the age. The brain is composed by highly differentiated cells that populate different anatomical regions and requires about 20% of body basal oxygen for its functions. Thus, it is not surprising that alterations in brain energy metabolisms lead to neurodegeneration.

Cellular energy is mainly produced via oxidative phosphorylation taking place within mitochondria, which are crucial organelles for numerous cellular processes, such as energy metabolism, calcium homeostasis, lipid biosynthesis, and apoptosis. Glucose oxidation is the most relevant source of energy in the brain, because of its high rate of ATP generation needed to maintain neuronal energy demands. Thus, neurons rely almost exclusively on the mitochondria, which produce the energy required for most of the cellular processes, including synaptic plasticity and neurotransmitter synthesis.

Reactive oxygen species (ROS) are normally produced in the cell of living organisms as a result of normal cellular metabolism and are fundamental in the maintenance of cellular homeostasis. When an imbalance between ROS production and detoxification occurs, ROS production may overwhelm antioxidant defenses, leading to the generation of a noxious condition called oxidative stress and overall to the impairment of the cellular functions. This phenomenon is observed in many pathological cases involving mitochondrial dysfunction, as well as in aging. The brain is particularly vulnerable to oxidative stress and damage, because of its high oxygen consumption, low antioxidants defenses, and high content of polyunsaturated fats very prone to be oxidized.

Mitochondrial dysfunction is one of the main features of the aging process, particularly in organs requiring a high-energy source such as the heart, muscles, brain, or liver. Although a large amount of data support the role of mitochondrial ROS production in aging, it has also recently been demonstrated the involvement of the mitochondrial permeability transition in the mechanisms of aging. The age-associated decrease in mitochondrial membrane potential correlated with reduced ATP synthesis in tissues of old animals. The mitochondrial permeability transition is due to a nonspecific pore called the mitochondrial permeability transition pore (mPTP) occurring when mitochondria become overloaded with calcium. Indeed, it is well known that aging alters cytosolic calcium pick-up and the sensitivity of the mPTP to calcium enhanced under oxidative stress conditions.

Neurons are postmitotic highly differentiated cells with a lifespan similar to that of the whole organism. These excitable cells are more sensitive to the accumulation of oxidative damages compared to dividing cells and are more prone to accumulating defective mitochondria during aging. Thus, it is not surprising the importance of protecting systems, including antioxidant defenses, to maintain neuronal integrity and survival. All the neurodegenerative disorders share several common features, such as the accumulation of abnormally aggregated proteins and the involvement of oxidative damage and mitochondrial dysfunction. Many of the genes associated with Parkinson’s disease or ALS are linked to mitochondria. In addition, all aggregated misfolded proteins (β-amyloid, tau, and α-synuclein) are known to inhibit mitochondrial function and induce oxidative stress. Therefore, the identification of common mechanisms underlying neurodegenerative diseases, including mitochondrial dysfunction, will increase our understanding of the essential requirements for neuronal survival that can inform future neuroprotective therapies.


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The Cosmological Noocene

The Cosmological Noocene

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Here is a sketch of the future, without any specific dates assigned to its milestones. The molecular biochemistry of living beings is fully mapped and understood. The human mind is reverse engineered. It is run in software. A million variants and improvements are constructed. Molecular nanotechnology is established and becomes a mature industry, available to everyone. Anything and everything can be built efficiently and at next to zero cost given the raw materials and a specification. All disease is abolished, and aging is defeated: these are problems that boil down to control over molecules, just another form of maintaining a machine to remove wear. The future stretches out indefinitely for all living entities, whether biological or otherwise. Given that, is perhaps never too early for at least a little long-term thinking, even though we’re still here in the present, working away at the very first rung of this tall ladder to the future.

From an economic perspective those who thrive in the era of molecular manufacturing and comprehension of mind are those who make the most efficient use of the matter that they own, and those who gain control over the most matter: quality versus quantity shift back and forth in the degree of advantage as the ability to accurately and rapidly manipulate large masses of matter at the atomic level and lower grows. Matter is most economically efficient when incorporated as the workings of an intelligent entity. The end state here is a continuum of thinking matter, and there are countless arrangements by which matter might be made aware. Our evolved biology is among the least intricate and least capable of these possibilities. At the most efficient we might envisage space- and matter-efficient computational processors plus the necessary workings for support: communication, energy, repair, and so forth. The higher the fraction of that mix that can be devoted to data processing and transfer, the more economically effective the entities who use that system as a substrate.

Evolved intelligences are not rational actors in search of growth above all other goals. We have parks and entertainment industries, for example. There is no reason why constructed or augmented intelligences should be any different, but equally they have one important quality: they can change themselves and their progeny in defined ways to achieve defined outcomes in mental state. The alterations and experiments that provide economic advantages will prosper. Entities who choose to incorporate an urge to growth will become the majority. At some point the value of an asteroid, a moon, a planetary crust, or a star in its natural state falls below the value of the same matter dismantled and used as raw materials for computational processing. After that it is just a matter of time before this solar system, a wilderness at present, and a collection of parks in ages ahead, is transitioned into a more efficient arrangement of matter in which near every portion of the whole is intelligent. This change will propagate outward to other stellar systems, without end, driven by simple economic considerations. A sea of cultures of a complexity and scope beyond our imaginings, and our world today the tiniest mote of a seed, that could be emulated by the smallest discrete material unit of computational processing in that future substrate.

So it is less a matter of manifest destiny that we will convert our entire future light cone into intelligence, and more a matter of economic inevitability, the destination at the end of the random walk of choice simply because some classes of choice will be made more frequently than others. The outcome of human action writ large, for a very expansive definition of the word human. All of this, however, indicates that there is something very important that we at present do not understand about the nature of reality. Nothing in our present situation as a species appears to be exceptional: stars are everywhere in vast numbers, planets also, and complex organic molecules are seen wherever we have the ability to observe them. Thus intelligence should arise elsewhere. The age of the universe is very long in comparison to the time taken for our spontaneous generation, yet we see no evidence that any other intelligence has come before us. This is often expressed as the Fermi Paradox, but is perhaps best thought of as the Wilderness Paradox, which is to ask why everything we observe, out to the very limits of the visible universe, is apparently natural and unaltered. Where are the signs of what we know is possible and inevitable for an intelligent evolved species, the conversion of matter to more efficient forms on a vast scale?

The only self-consistent solution to the Fermi Paradox that does not require some new and presently missing piece of scientific understanding is the Simulation Argument: that we are in a box and walled off from the real world, whatever that might be, created by some demiurge for purposes guessable but ultimately unknowable through any action on our part. Prosaically that demiurge might be a descendant of a past humanity similar to ours, an entity that is running one of countless ancestor simulations for scientific reasons. Far less prosaic options are also possible, in which the demiurge is simulating from first principles a radically different cosmology from its own and thus its nature and motivations are inscrutable. These possibilities of the Simulation Argument are dissatisfying to explore, however, for all the same reasons as the brain in a jar thought experiment is a dead end. Best to assume it is not true, as it if is there is nothing useful you can do about it, individually or collectively. It is Pascal’s Wager turned inside-out.

It is more interesting to speculate on what it is that we don’t understand at present about the nature of reality. There are numerous candidates, and most present thinking is directed towards those related to enforcing our rarity, often expressed as the Great Filter, one or more enormously unlikely steps that lie between the origin of a barren world scattered with a few organic compounds and the destination of an intelligent species engaged in repurposing of raw materials on a vast scale. All proposed Great Filters are very speculative; there is a great deal of room to argue about odds when you only have one example to work with, or events of the distant past must be reconstructed from theory, or future development of the species considered in detail rather than at a very high level, all which makes coming to any sort of rigorous conclusion next to impossible. All that is practical to achieve is to build the shape of the argument that would be sufficient if the actual numbers and proposed events in fact exist in reality. Given this uncertainty, any proposed Great Filter becomes an ever less satisfying answer the further we look outward and the more galaxies we see without any sign of massive engineering. It only serves to argue for our uniqueness, which is implausible given what we presently know and the isotropic nature of all other observed aspects of the natural universe across vast spans of distance and time.

Per our present understanding of physics and intelligent economic activity, we will turn every part of that great span, stars and all, into our descendants if not diverted or stopped by some outside influence. The cosmological noocene, an ocean of intelligence of breathtaking scope and grandeur. That the natural universe remains as it is to be used by us indicates that something is awry, however, that some vital and important understanding is missing. We as a species are still in the act of making the first fumbling explorations of the bounds of the possible with regards to what it is that we don’t know.

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Recognizing the signs and symptoms of sepsis

Recognizing the signs and symptoms of sepsis

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Sepsis is a life-threatening condition triggered by a systemic infection, ultimately affecting the function of your vital organs. The infection is sometimes referred to as “blood poisoning” by the public. According to a study tracking data in two different hospital cohorts, 34.7% to 55.9% of American patients who died in hospitals between 2010 and 2012 had sepsis at the time of their death, depending on which inpatient cohort they were in.1

The condition does not discriminate and affects all age groups, socioeconomic groups and genders. A successful outcome relies on early detection and rapid treatment.

Experts are calling for recognition2 of sepsis as a distinct cause of death, hoping this will result in better clinical practice guidelines, stressing awareness in the community and the ER, which may reduce the overall number of deaths.

Infections that progress to sepsis in the hospital may increase risk of death. Researchers found the death rate of patients with sepsis was 10% compared to 1% among patients without sepsis.3 In fact, the same study found half of all in-hospital deaths were related to sepsis.

According to the Centers for Disease Control and Prevention,4 each year 1.7 million adults in the U.S. will develop sepsis and nearly 270,000 will die as a result. In a study5 published in 2016, researchers found sepsis was the most expensive condition treated in the U.S., costing $23.6 billion each year.6

The study discovered total hospital care costs had remained stable but spending for sepsis rose by 19% from 2011 to 2013.7 Data showed sepsis was responsible for 6.2% of all hospital costs across the U.S. and hospitalization for sepsis was 70% more expensive than the average stay. Learning to recognize the symptoms to seek early care may improve the potential for a successful outcome.

Mother recognized sepsis symptoms and sought medical care

One mother in the U.K. made the decision to take her son to the emergency room after he scraped his arm at the zoo the week before. Alexandra Ruddy shared with Yahoo Lifestyle the story of how her son fell at the zoo and scraped his arm.8 Once home she cleaned the wound and cautioned him to continue to wash his hands and take care of the injury throughout the week.

Although the wound didn’t look infected to her, she noticed it had gotten bigger. On the way to the beach over the weekend, she noticed red track marks on his arm. She brought her son to urgent care where the physician commended her for bringing her son in quickly, as9 “It isn’t something you can ‘leave’ until Monday when the doctors are back in the office.”

Luckily, early recognition and treatment contributed to her son’s recovery. She credits knowing about what to look for from information she received from a friend two years earlier. But, sepsis may not always present after an injury or scrape.

Psychotherapist Dean Rosen thought he had the flu when he woke up with a fever.10 Less than 12 hours later, after his wife had driven him to the hospital, the emergency room physician told him he was septic and going into shock. Rosen’s blood pressure plummeted, and his kidneys shut down.

To save him, hospital staff put a port into his neck and pumped in vasoconstrictors and antibiotics. In Rosen’s case, scar tissue from Crohn’s disease had created a blockage in his intestines, resulting in an infection. Rosen was on medication for his Crohn’s disease that weakened his immune system and increased his risk.11

What is sepsis?

Sepsis is an extreme response to an infection already present in your body.12 The result is a medical emergency from a life-threatening chain reaction. According to the Sepsis Alliance,13 80% of cases start in the community and not in the hospital.

The most common types of infection triggering sepsis and/or septic shock are respiratory or urinary tract infections.14 However, sepsis may also develop with an infected cut or scrape as it did for Ruddy’s son, or strep throat, just to name a few scenarios.

Like Rosen, you may not even be aware that you have an infection, although most typically are.15 The definition of sepsis is a16 “life-threatening organ dysfunction caused by a dysregulated host response to infection.” As explained by the National Institute of General Medical Sciences:17

“Sepsis … is caused by an overwhelming immune response to infection. The body releases immune chemicals into the blood to combat the infection. Those chemicals trigger widespread inflammation, which leads to blood clots and leaky blood vessels. As a result, blood flow is impaired, and that deprives organs of nutrients and oxygen and leads to organ damage.

In severe cases, one or more organs fail. In the worst cases, blood pressure drops, the heart weakens, and the patient spirals toward septic shock. Once this happens, multiple organs — lungs, kidneys, liver — may quickly fail, and the patient can die.”

Symptoms of sepsis may look like something else

One of the most important steps you can take to protect your health is to recognize the symptoms of sepsis and seek immediate medical attention if you suspect sepsis.

It is important not to make a diagnosis at home, but instead communicate your concerns with a medical professional who may begin immediate treatment. The signs of sepsis may be subtle and could be mistaken for other conditions. However, sepsis often produces:18,19,20

A high fever with chills and shivering

Rapid heartbeat (tachycardia)

Rapid breathing (tachypnea)

Unusual level of sweating (diaphoresis)


Confusion or disorientation

Slurred speech

Diarrhea, nausea or vomiting

Difficulty breathing, shortness of breath

Severe muscle pain

Low urine output

Cold and clammy skin

Skin rash

Many of these symptoms may be confused with a bad cold or the flu. However, they tend to develop quicker than you would normally expect. The Sepsis Alliance recommends using the acronym TIME to remember some of the more common symptoms:21

  • T — Temperature higher or lower than normal?
  • I — Have you now or recently had any signs of an infection?
  • M — Are there any changes in mental status, such as confusion or excessive sleepiness?
  • E — Are you experiencing any extreme pain or illness; do you have a “feeling you may die?”

Know the causes and risk factors of sepsis

While viruses, fungi and parasites may all trigger sepsis, bacterial infections are currently the most common cause. However, research22 has demonstrated the number of fungal-induced sepsis infections is on the rise. There are several conditions that may raise your risk of developing sepsis, including:23,24


Cancer and chemotherapy

HIV infection


Chronic illness

Urinary tract infections

Advanced age

Premature infants

Spleen removal

The rising number of antibiotic-resistant infections is also cause for concern as these infections are capable of triggering sepsis. The most commonly known antibiotic-resistant bacteria are methicillin-resistant Staphylococcus aureus (MRSA), which was first discovered in 1961.25 Over the years, newer drugs treated MRSA for a short time until the bacteria again became resistant.

The growth of antibiotic resistance is a major threat to public health worldwide, and a primary cause for this man-made epidemic is the misuse of antibiotics.26 Your exposure to antibiotic overuse is not just from prescriptions in the doctor’s office but also in food production.

Agricultural use accounts for 80% of all antibiotics used in the U.S.,27 which ultimately affects those who eat the meat from animals raised in concentrated animal feeding operations. The antibiotics alter the gut microbiome in the animal, making some antibiotic-resistant. These pass into the environment through the manure or contaminate the meat during slaughter or processing.

Post sepsis syndrome

While some will recover fully from sepsis, for many the problems do not end at discharge from the hospital. Survivors may suffer physical, psychological and/or neurological consequences for the rest of their lives. The combination of symptoms is called post sepsis syndrome and usually last between six and 18 months. Symptoms of post sepsis syndrome may include:28,29

Lethargy (excessive tiredness)

Changes in peripheral sensation

Repeated infections at the original site or a new infection

Poor mobility

Muscle weakness

Shortness of breath

Chest pains

Swollen limbs

Joint and muscle pains


Hair loss

Dry flaking skin and nails

Taste changes

Poor appetite

Changes in vision

Difficulty swallowing

Reduced kidney function

Feeling cold

Excessive sweating




Post-traumatic stress disorder

Poor concentration

Short-term memory loss

Mood swings

Clouded thinking



Currently, there is no specific treatment for post sepsis syndrome, but most get better over time. The U.K. Sepsis Trust30 recommends managing individual symptoms and supporting optimal health as you’re recovering. They encourage survivors to talk with friends and family and not to suffer with their symptoms in silence, as this helps to get through the difficult time.

Not all medical professionals are aware of post sepsis syndrome, so it may be helpful to talk about your symptoms and ask for a referral to someone who may help manage your mental, physical and emotional challenges. Some survivors find their immune system is not as effective as long as a year following their recovery, resulting in one infection after another, including coughs and colds.

Vitamin C — A game changer in sepsis treatment

Unfortunately, treatment for sepsis is a considerable challenge, and becoming more so as antibiotic-resistant infections become more prevalent. In the video above, Dr. Paul Marik, chief of pulmonary and critical care medicine at Sentara Norfolk General Hospital in East Virginia, discusses a successful treatment protocol he developed.

Marik’s first patient, a 48-year-old woman with a severe case of sepsis, presented in January 2016. Marik describes her condition, saying, “Her kidneys weren’t working. Her lungs weren’t working. She was going to die.”

Having read a study by researchers who had experienced moderate success treating individuals with sepsis using intravenous vitamin C, he decided to give it a try and added hydrocortisone to the infusion. Marik expected his patient would not survive the night, and was surprised to find her well on the road to recovery the next morning.

For the first two or three patients, only vitamin C and hydrocortisone were used. Marik then decided to add thiamine, for several reasons. Importantly, it’s required for metabolism of some of the metabolites of vitamin C, it protects the kidneys from failure common in sepsis,31 and many presenting with sepsis are thiamine deficient.32

Marik’s retrospective before-after clinical study published in the journal Chest,33 showed giving patients intravenous vitamin C with hydrocortisone and thiamine (vitamin B1) for two days reduced mortality nearly fivefold, from 40.4% in the control group receiving standard treatment, to 8.5% in the experimental group.

Developing an effective treatment could reap billions of dollars. However, in this case, profit is not the motive as the cost of ingredients for the protocol are as little as a single dose of antibiotics.

Consider these strategies to reduce your risk of sepsis

Part of what makes sepsis so deadly is people typically do not suspect it, and the longer you wait to treat it, the deadlier it gets.34 If you develop an infection, stay alert to symptoms of sepsis and seek immediate medical attention if they appear. Even health care workers can miss the signs and delay treatment. You may lower your own risk by:

Supporting your immune system — Sleep, nutrition, exercise and optimizing your gut microbiome are foundational pillars of health. You’ll find simple strategies to support those systems in the following articles:

Caring for any chronic illness affecting your risk of sepsis — Research has found illnesses that increase your risk may include chronic lung disease, chronic kidney disease, diabetes, stroke and cardiovascular disease.35

Promptly treating urinary tract infections (UTIs) — UTIs are the second most common type of infection in the body, diagnosed in 150 million people each year worldwide,36 and one of the common reasons for the development of sepsis.37

Conventional treatment typically involves antibiotics, but research shows that UTIs caused by E. coli — which comprise38 90% of all UTIs — can be successfully treated with D-Mannose,39 a naturally occurring sugar that’s closely related to glucose. To learn more, see “D-Mannose for UTI prevention validated in a clinical trial.”

Properly cleaning skin wounds — Always take the time to properly clean and care for wounds and scrapes. Wash the open area with mild soap and water to and cover with a sterile bandage. Diabetics should follow good foot care to avoid dangerous foot infections.

Avoiding infections in hospitals — When visiting a health care facility, be sure to wash your own hands, and remind doctors and nurses to wash theirs (and/or change gloves) before touching you or any equipment being used on you.

Stopping nail biting — One study found 46.9% of the participants participated in nail biting (onychophagia).40 Exposure of the delicate skin underneath the nail, transferred from your mouth or acquired from the environment, increases the risk of infection.

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Corn oil — Important caveats to remember

Corn oil — Important caveats to remember

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Warning: This oil comes with potentially damaging side effects due to either the ingredient it’s made from or the manufacturing process used to extract it. Because these negative effects overshadow the potential benefits, I do not recommend this oil as a food or for therapeutic use. Always be aware of the potential side effects of any herbal oil before using.

Food nutrients are highly sensitive to heat,1,2 so there are several factors to consider when cooking to preserve as much of these nutrients as possible. One of these factors is the cooking oil you use.

Some cooking oils are stable enough to resist chemical changes when heated to high temperatures, while other oils, like polyunsaturated vegetable oils, can increase the risk for heat-induced damage and create high-energy molecules called free radicals upon degrading inside your body.3,4 One of the most popular vegetable oils is corn oil. Discover the health risks of using corn oil for cooking and whether this oil is good for any other purpose.

What is corn oil?

Corn or maize oil is extracted from the germ of corn. It’s mainly used for cooking and is also a key ingredient in margarine and other processed foods.5 Corn oil is also used in various industrial applications, such as stock for biodiesel6 and a constituent in the production of resins, plastics and lubricants, to name a few.7

Despite being generally less expensive than other vegetable oils on the store shelf,8 a huge factor in its price is the staggering amount of subsidies the United States gives to corn to underwrite the cost. Corn is one of the most heavily subsidized crops in the country, raking in over $111.2 billion from the government between 1995 and 2017, according to data from the Environmental Working Group (EWG).9

As you can see, this subsidy on a basically unhealthy food easily undersells healthy choices. A study published in the Journal of the American Medical Association shows that the high consumption of foods derived from subsidized commodities like corn is associated with an increased risk of cardiometabolic disease in adults.10

Moreover, the problem with using corn oil and other vegetable oils for cooking is that they contain perishable bonds that create free radicals in the presence of oxygen, a process also known as autoxidation.11 These free radicals can lead to cholesterol oxidation, which has been linked to an increased risk of diseases such as atherosclerosis, Alzheimer’s disease, retinal degeneration, age-related macular degeneration and cataracts.12

Corn oil also contains very high amounts of omega-6 fats, which can throw your body’s omega-6 to omega-3 ratio out of balance. Corn oil is reported to have an omega-6 to omega-3 ratio of 46-to-113 — a far cry from the ideal 1-to-1 ratio. The standard American diet already has far too much omega-6 in it, and the serious distortion of the ratio further increases your risk for many degenerative diseases.14

Uses of corn oil

Apart from serving as a less-than-ideal cooking oil, corn oil is used in manufacturing paint, ink, textiles and insecticides.15 It also sometimes functions as a carrier oil for drug molecules in pharmaceutical products.16

Corn oil is used for skin care products as well, including soaps, balms and other bathing essentials.17 You can also massage it onto your scalp to help strengthen and add shine to your dry hair.18 Here are some of the ways you can use corn oil around your home:

  1. Lubricate a key lock — If you have a sticky key lock at home, wipe the key with corn oil before inserting it into the lock. The oil acts as a lubricant, making it easier for you to turn and pull out the key.19
  2. Clean up watermarks from wooden furniture — Mix equal parts of salt and corn oil then rub it onto the watermarks on your wood furniture. Use a clean cloth to polish it off.20
  3. Coat your snow shovel — Rubbing the oil on your shovel will prevent snow from sticking to it.21

Composition of corn oil

According to the United States Department of Agriculture, industrial and retail corn oil contains 27.5 grams of total monounsaturated fats, 54.6 grams of total polyunsaturated fats and 12.9 grams of total saturated fats per 100-gram serving.22

One important caveat you need to consider regarding this oil is that it’s typically derived from genetically modified (GM) seeds that are designed to resist herbicides like glyphosate.

A study published in the International Journal of Biological Sciences demonstrates the toxicity of three GM corn varieties from biotech company Monsanto, now Bayer. Results show that consuming GM corn increases the risk for hepatorenal toxicity and unintended direct or indirect metabolic consequences.23

How corn oil is made

To extract corn oil from the corn germ, a combination of continuous screw presses and solvent extraction is used. The initial expeller extracts around 50% of the oil content, while the solvent extraction brings the total yield to 95%. The corn oil is then refined through degumming to remove phosphatides, alkali treatment to neutralize free fatty acids and bleaching to remove trace elements and create a desirable color.

The final steps of the refining process include winterization, a process wherein high melting waxes are removed, and deodorization.24 This entire process may contribute to the potential health risks of corn oil.25

How does corn oil work?

When used for cooking, corn oil serves as a medium in which heat can be transferred. It may also help contribute to the flavor and texture of food.26 However, I do not recommend using corn oil for cooking, as it can potentially lead to a variety of health problems. For practical uses, such as for aromatherapy, skin conditioning or hot oil massage, corn oil works as a carrier oil.27

Is corn oil safe?

Corn oil and other polyunsaturated vegetable oils are heavily marketed for “healthful” cooking alongside the vilification of saturated fats, which actually do not cause heart disease and, on the contrary, serve as a healthful addition in your diet.28 Aside from the oxidized oil dangers I discussed in the first section, here are two other issues you should be aware of with corn oil and vegetables oils:

  1. The majority of these vegetables oils in the U.S. are made from genetically modified crops,29 which can contain residues of the herbicide glyphosate and Bt toxin found in GM corn and soy.
  2. They are heavily processed, potentially causing a range of ill health consequences.30

Side effects of corn oil

Some of the worst foods you can consume are those cooked with polyunsaturated vegetable oils like corn oil.31 The introduction of oxidized cholesterol into your system is a big concern, converting your good cholesterol into bad, which leads directly to cardiovascular diseases.32

When heated, corn oil produces harmful chemicals called aldehydes, which have been found to increase the risk for autism spectrum disorder, Parkinson’s disease and gastric, breast and prostate cancer.33 A study published in the Journal of Lipid Research also shows that polyunsaturated fatty acids promote hepatic inflammation.34

If you’re looking for a cooking oil that is less susceptible to heat-induced damage and will not put you at risk of various chronic diseases, consider using coconut oil. Coconut oil contains healthy fats that may help support your heart health,35 thyroid function,36 immune system,37 brain function38 and metabolism,39 among others.

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Temporary β-catenin Inhibition Attenuates Effects of Aging on Bone Regeneration

Temporary β-catenin Inhibition Attenuates Effects of Aging on Bone Regeneration

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For all that it reports a success, the open access paper here is an excellent example of the prevalent, inferior approach to the development of therapies for age-related conditions. Instead of looking for causes of the problem in question, the slow and dysfunction regeneration of bone fractures in older individuals, the scientists find a way to tinker with the dysfunctional state of aged metabolism, overriding one of the detrimental regulatory changes to some degree. As a strategy this will always be far less effective than tackling the underlying root causes of age-related dysfunction: trying to tinker a damaged engine into continued operation without fixing the damage is always going to be a challenging task. Nonetheless, this strategy remains much more popular in the research community, more is the pity.

Almost a third of humans will fracture a bone, and most often these injuries go on to successfully heal. However, various environmental and biological factors can hinder this regenerative process. With age, the pace of fracture repair slows, and the risk of non-union increases. This slower pace of repair in older individuals is responsible for increased morbidity and even mortality.

While there are many factors that could impair fracture healing with aging, the pace of fracture repair can be rejuvenated by circulating factors present in young animals. Recent data suggests that factors produced by young macrophage cells pay a critical role in the rejuvenation process. While these factors regulate the pace of repair, their effects on mesenchymal cells differentiating to osteoblasts are mediated by signaling pathways such as β-catenin.

β-catenin signaling plays different roles in mesenchymal differentiation at different repair stages. In the initial phase of repair, the level of β-catenin needs to be precisely regulated as levels that are too high or too low will prevent undifferentiated mesenchymal cells from becoming osteochondral progenitors and will inhibit fracture healing. Once the cells differentiate to osteochondral progenitors, higher levels of β-catenin stimulate osteogenesis and enhance fracture repair.

Here we examined the ability of pharmacologic agents that target β-catenin to improve the quality of fracture repair in old mice. 20 month old mice were treated with Nefopam or the tankyrase inhibitor XAV939 after a tibia fracture. Fractures were examined 21 days later by micro-CT and histology, and 28 days later using mechanical testing. Daily treatment with Nefopam for three or seven days but not ten days improved the amount of bone present at the fracture site, inhibited β-catenin protein level, and increased colony forming units osteoblastic from bone marrow cells. This data supports the notion that high levels of β-catenin in the early phase of fracture healing in old animals slows osteogenesis, and suggests a pharmacologic approach that targets β-catenin to improve fracture repair in the elderly.


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A Discussion of Mitochondrial DNA Damage and Aging

A Discussion of Mitochondrial DNA Damage and Aging

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Every cell in the body contains a swarm of mitochondria, responsible for packaging the chemical energy store molecule ATP that is used to power cellular processes. Mitochondria are the distant descendants of symbiotic bacteria, and retain a remnant of the original DNA. This mitochondrial DNA is unfortunately less well protected and maintained than DNA in the cell nucleus. It is thought that a sizable fraction of the declines of aging are caused by accumulated damage to mitochondrial DNA, coupled with progressive failure of the quality control mechanisms responsible for recycling dysfunctional mitochondria. Reducing the functional capacity of cells via a reduction in available energy can produce all sorts of detrimental effects, and while much of the relevant research is focused on the energy hungry tissues of brain and muscle, this is a problem in all tissues.

The mitochondrial organelle, a double-membraned organelle with its evolutionary origins in the eubacterial kingdom, is the central factor in the energy metabolism of the eukaryotic cell. It is responsible for the vast majority of the ATP (adenosine triphosphate) produced in the cell (~90% under normal circumstances), which it produces through oxidative phosphorylation (OXPHOS) by way of a multi-subunit complex called the electron transport chain (ETC). The mitochondrion possesses its own small, circular genome (mtDNA) that encodes key RNA and proteins required for OXPHOS.

The mtDNA mutation rate depends on many factors, including the extent of oxidative stress and the fidelity of the mitochondrial DNA polymerase (POLG). The production of reactive oxygen species (ROS) is an inevitable outcome of the oxidative phosphorylation process that occurs within the mitochondrion, and these chemical byproducts are, by their nature, damaging to DNA. Thus, given its proximity to the source of ROS production, mtDNA experiences a high rate of ROS-induced mutation. ROS production is also increased by pre-existing mtDNA damage, excess calories, regional mtDNA genetic variations, and alterations in nuclear DNA expression of stress response genes, creating a vicious cycle where increased ROS production can encourage the occurrence of even more ROS production over time.

There is a well-established correlation between aging and a decline in mitochondrial function, which likely contributes to age-related senescence and geriatric disease. PolgD257A “mutator” mice – which exhibit increased mtDNA mutation rates – show an accelerated aging phenotype, suggesting that the accumulation of mtDNA mutations over time may be a crucial factor driving the aging of mammals. The age-related decline in mitochondrial function is likely caused, in large part, by the gradual accumulation of somatic mtDNA mutations due to ROS damage and DNA replication errors. This accumulation of mtDNA mutations promotes even more ROS production, establishing a vicious cycle and accelerating the aging process. Although a serious mtDNA mutation can be acquired early in life, for most people it will take several decades to acquire one or more disease-causing mutations and have them reach a sufficiently high level of heteroplasmy to cause serious health issues. This gradual accumulation of mutations and increase in heteroplasmy may help explain the time-dependent decline in function that occurs with age.

Somatically-acquired mtDNA mutations can occur anywhere in mtDNA and may even include large deletions or duplications. Loss of mtDNA integrity (by altered mtDNA copy number or increased mutations) has been implicated in cellular dysfunction with aging. Deletion mutations are an insidious risk because the reduced size of mtDNA molecules carrying large deletions (ΔmtDNAs) gives them a replicative advantage over normal mtDNA.

Any mtDNA molecules containing a deleterious mutation in a coding gene, combined with a D-loop mutation that creates a strong proliferative advantage, would have the potential to create severe issues in old age, particularly if they cause the cell to take on neoplastic properties. Furthermore, this ubiquitous and steadily accumulating mutational load in the mtDNA population will likely create general problems for the ETC function and mitochondrial health, thus contributing to age-related senescence. For these reasons, we believe there is great merit in the argument that mitochondrial defects play a significant role in the development of many common diseases of age. We hypothesize that the diversity of mutations in mtDNA could be decisive for the variability of clinical phenotypes, such as age of disease onset.


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Rejuvenation Biotechnology Companies Presenting at Biotech Investing in Longevity, in San Francisco May 2019

Rejuvenation Biotechnology Companies Presenting at Biotech Investing in Longevity, in San Francisco May 2019

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Aikora Health and Foresight Institute recently collaborated to host a gathering of investors, entrepreneurs, and supporters from the core rejuvenation biotechnology community. The event was held in San Francisco, and I attended to present a summary of ongoing work at Repair Biotechnologies. It was an interesting mix of local folk and visitors from across the US, a chance to catch up with fellow travelers from other companies and some of our investors. As you probably know, the SENS Research Foundation and a number of influential aging research institutions, such as the Buck Institute, are based in the Bay Area. It has long been the case that the venture and technology communities in California include many people sympathetic to the SENS goal of bringing aging under medical control – it isn’t a coincidence that the SENS Research Foundation set up their research center in this part of the world.

The presentations were recorded, and in the video here see my outline in addition to those by principals at the Methuselah Fund, Leucadia Therapeutics, and As you might recall, Repair Biotechnologies is working on reversal of atherosclerotic lesions, aiming to prevent the contribution of this condition to late life mortality, and regrowth of the thymus, so as to restore the pace of creation of T cells, and improve immune function in later life. We recently raised our seed round, so we’re hard at work in the lab at the moment.

The other two biotech companies are working on very interesting projects, and I’ve mentioned both in the past here at Fight Aging! In the case of Leucadia, you might look at the presentation given by Doug Ethell at Undoing Aging 2018 for a good overview of the company and its approach. It is exactly the sort of radically different, cost-effective approach to Alzheimer’s disease that we’d like to see more of. is equally radical in the goal of a href=””>transiently reprogramming cells in vivo, spurring them into the improvements observed in the reprogramming of somatic cells into induced pluripotent cells: repair of mitochondrial function, possibly repair of other molecular damage, and reversion of epigenetic markers of aging. There should be more of this sort of ambition in evidence in the biotechnology community.

Methuselah Fund, Leucadia Therapeutics, Turn Biotechnologies and Repair Biotechnologies

Four presentations at “Biotech Investing in Longevity” on 1st May 2019 in San Francisco: Sergio Ruiz – Methuselah Fund; Doug Ethell – Leucadia Therapeutics; Vittorio Sebastiano – Turn Bio; Reason – Repair Biotechnologies.

The Methuselah Fund is designed to accelerate results in the longevity field, extending the healthy human lifespan. They measure their success not just by financial return-on-investments but also by what they call return-on-mission. Their DNA stems from The Methuselah Foundation, which has been working hard during the last 18 years to make 90 the new 50 by 2030.

Leucadia Therapeutics is determined to end Alzheimer’s disease with Arethusta, a first-in-class treatment for mild cognitive impairment associated with Alzheimer’s disease. Cerebrospinal fluid (CSF) clears toxic metabolites from intercellular spaces in the brain, much as the lymphatic system does in the rest of the body. The first regions of the brain to be impacted by Alzheimer’s disease are cleared by CSF that drains across a porous bone called the cribriform plate. Aging and life events can occlude the cribriform plate and reduce the CSF-mediated clearance of toxic metabolites from those regions of the brain, thereby causing plaques and tangles formation. Leucadia’s patented Arethusta technology restores CSF flow across the cribriform plate, improving the clearance of toxic metabolites from the earliest regions of the brain to be affected by Alzheimer’s disease. develops a transient reprogramming protocol that has demonstrated a youthful reversion of eight of the nine hallmarks of aging. Reversion of the ninth is being currently being developed. They technology has already been proven to rejuvenate five different tissue types of the human body with more being evaluated. Osteoarthritis, skin damage, and sarcopenia are all proven targets of the technology, with other indications soon to be tested.

Repair Biotechnologies is a longevity company with the mission to develop and bring to the clinic therapies that significantly improve human healthspan through targeting the causes of age-related diseases and aging itself. The company currently runs two preclinical development programs: the first for thymus regeneration and immune system restoration, and the second for reversal of atherosclerosis.

Aikora Health and Foresight Institute joined forces to organize a series of talks on biotech investment and longevity. They gathered a curated group of entrepreneurs, scientists, and investors to discuss exciting projects that seek to extend human healthspan, surveying a diversity of novel approaches, and discussing which ambitious goals are realistically within our reach.

Aikora Health connect investors with companies, founders and scientists in the health tech, genomics, and regenerative medicine sectors. Our key focus is on longevity tech with the potential to transform healthcare and human aging. We offer insight and information regarding the biotech and increasingly important longevity space, in addition to matching founders of biotech and longevity companies with funding and strategic partnerships.

Foresight Institute is a leading think tank and public interest organization focused on emerging world-shaping technologies. It was founded in 1986 on a vision of coming revolutions in technology that will bring extraordinary opportunities, as well as unprecedented challenges. Foresight’s mission is to steer towards positive futures, futures of Existential Hope.

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Suggesting that Cytomegalovirus Infection Contributes to Metabolic Syndrome

Suggesting that Cytomegalovirus Infection Contributes to Metabolic Syndrome

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Metabolic syndrome is the precursor to type 2 diabetes, and is caused by the presence of excess visceral fat tissue. Age is a factor, however, in that people become more susceptible to the harmful consequences of being overweight in later life. Why is this the case? Recent evidence points towards the creation of additional lingering senescent cells as an important mechanism linking fat tissue to chronic inflammation and disruption of metabolism. Cellular senescence is an age-related mechanism.

cytomegalovirus (CMV) infection. CMV is very prevalent, and the consensus on its effects is that its presence is an important contribution to the decline of the immune system with advancing age. Too many immune cells become specialized to tackling CMV, leaving too few for other tasks. In the context in which the supply of new immune cells is greatly diminished, due to loss of thymic tissue, and declining activity of hematopoietic stem cells, this is a big problem.

Cytomegalovirus (CMV) is a ubiquitous herpesvirus infecting most of the world’s population. CMV has been rigorously investigated for its impact on lifelong immunity and potential complications arising from lifelong infection. A rigorous adaptive immune response mounts during progression of CMV infection from acute to latent states. CD8 T cells, in large part, drive this response and have very clearly been demonstrated to take up residence in the salivary gland and lungs of infected mice during latency. However, the role of tissue resident CD8 T cells as an ongoing defense mechanism against CMV has not been studied in other anatomical locations.

Therefore, we sought to identify additional locations of anti-CMV T cell residency and the physiological consequences of such a response. Through RT-qPCR we found that mouse CMV (mCMV) infected the visceral adipose tissue and that this resulted in an expansion of leukocytes in situ. We further found, through flow cytometry, that adipose tissue became enriched in cytotoxic CD8 T cells that are specific for mCMV antigens from day 7 post infection through the lifespan of an infected animal and that carry markers of tissue residence. Furthermore, we found that inflammatory cytokines are elevated alongside the expansion of CD8 T cells. Finally, we show a correlation between the inflammatory state of adipose tissue in response to mCMV infection and the development of hyperglycemia in mice.

Overall, this study identifies adipose tissue as a location of viral infection leading to a sustained and lifelong adaptive immune response mediated by CD8 T cells that correlates with hyperglycemia. This data potentially provides a mechanistic link between metabolic syndrome and chronic infection.


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A Better Understanding of the Mechanisms Surrounding Thymic Involution

A Better Understanding of the Mechanisms Surrounding Thymic Involution

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Researchers here report on their exploration of the protein interactions involved in the loss of active thymic tissue with age, a process called thymic involution. Since the thymus is where T cells mature, this loss contributes to the age-related decline of the adaptive immune system. Historically, this sort of investigation has focused on FOXN1 as the master regulator of thymic growth and activity. Upstream of FOXN1 is BMP4, however, and the paper here discusses the ways in which BMP4 is dysregulated with age. This discussion should probably be read in the context of other work that strongly suggests chronic inflammation is the driver of changes leading to thymic involution. Nothing happens in isolation in aging tissues, and there are usually deeper causes to be considered.

Thymic epithelial cells (TECs) are essential for the establishment of the specialized microenvironment that orchestrates the development of naive, self-tolerant T cells from hematopoietic precursors. They are supported by non-epithelial thymic stromal cells (TSCs), such as fibroblasts and endothelial cells, in an extracellular matrix-rich three-dimensional (3D) scaffold structure. TECs can be broadly divided into functionally and spatially distinct cortical (cTEC) and medullary (mTEC) subsets. Thymic epithelial progenitor cells (TEPC) support the development of both cTECs and mTECs during thymus organogenesis.

Deterioration of thymus function occurs naturally during aging and ultimately constrains the host immune repertoire. It is characterized by a reduction in total thymic cellularity and naive T cell production. Reduced TEC turnover and diminished levels of transcription factor forkhead-box N1 (FOXN1), a master regulator of TEC lineage specification, have been observed in the aged thymus. An increase in steroidal hormone production at puberty has also been implicated in age-related thymus involution, with androgen deprivation (AD) inducing the recovery of naive T cell production and bone marrow function in aged male mice and in humans. However, the mechanisms and signaling pathways causing the post-pubertal loss of specific TECs and underpinning AD-induced thymocyte regeneration remain unclear.

In this study, we examined numeric, phenotypic, and transcriptomic alterations in TEC and non-TEC (non-epithelial stromal cells, fibroblasts, and endothelial cells) stromal subsets during age-related thymic involution, and following transient thymic recovery via AD. We identify two major phases of thymic epithelial cell (TEC) loss during aging: a block in mature TEC differentiation from the pool of immature precursors, occurring at the onset of puberty, followed by impaired TEC progenitor differentiation and depletion of cTEC and mTEC lineage-specific precursors. We reveal that an increase in follistatin production by aging TECs contributes to their own demise. TEC loss occurs primarily through the antagonism of activin A signaling, which we show is required for TEC maturation and acts in dissonance to BMP4, which promotes the maintenance of TEC progenitors. These results support a model in which an imbalance of activin A and BMP4 signaling underpins the degeneration of postnatal TEC maintenance during aging, and its reversal enables the transient replenishment of mature TECs.


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