Researchers have demonstrated that “damaged muscle tissues treated with satellite cells in a special degradable hydrogel showed satisfactory regeneration and muscle activity. Muscle activity in repaired muscle in a mouse model was comparable with untreated muscles. … Satellite cells (SCs), freshly isolated or transplanted within their niche, are presently considered the best source for muscle regeneration. They are located around existing muscles. Hence, a patient’s own cells can be used, from a muscle biopsy. … A key issue for regeneration is how cells grow as a structure, as they usually require some form of framework. A hard framework would impede muscle growth and muscle cell penetration. The hydrogel, by contrast, provides a supportive structural skeleton but degrades quickly as muscle tissue returns and the support becomes unnecessary. The gel is initially liquid, hardens in place under UV light, and is easily penetrated by muscle cells. … This is using the patient’s own cells, without any lengthy culturing process, which means we could take a biopsy, produce the cells in a couple of hours, and implant them where needed – it can be done in theatre as one process. Using the patient’s own cells eliminates any tissue rejection. … The focus for initial clinical research in humans will be relatively small muscles at first, like deformities in the face and palate, or in the hand. It will be technically more demanding to grow larger muscles with more structure, which would require their own nerves and blood supply.”

Link: http://www.ucl.ac.uk/news/news-articles/1103/31031101

The present generation of therapies for rheumatoid arthritis are based on TNF inhibition – a fairly crude manipulation of the immune system when considered in the grand scheme of what is possible, but one that is getting better. From Technology Review: “A new protein engineered to inhibit molecules that cause inflammation not only reduces symptoms of rheumatoid arthritis in mice but also may have potential to reverse the disease’s course. Researchers hope the findings will point toward a new therapy for this crippling and difficult-to-treat disease, which occurs when the immune system attacks the body’s own joints. Even medications that are most successful in halting joint inflammation are effective in only about half of the patients who try them. … The new synthetic protein [appears] to target TNF in a far more specific fashion and could be produced at a small fraction of the cost [of present TNF inhibitors]. … a protein called progranulin binds to TNF receptors and that administering the protein to mice with rheumatoid arthritis reduced or even eliminated their symptoms. Then they determined which fragments of progranulin were responsible for binding to TNF and combined those fragments to engineer a protein that works even better to suppress disease. Mice with mild arthritis appeared to be disease-free after several weeks of regular injections of the modified progranulin.”

Link: http://technologyreview.com/biomedicine/35091/

Do you remember how you felt and thought when you were 17 or 18? No, I’m not just talking about your adolescent obsession with your sexuality – I mean the feeling that the world was yours to conquer! Don’t you remember that drive and ambition you had, that feeling that you could do just about anything? We all felt invincible and immortal at that age.

Your youthful optimism was not born merely out of naiveté and inexperience. In fact, that energetic, optimistic drive to conquer the world was largely a product of hormones – yes, those same raging hormones that drove your newly discovered sexuality. Most of the important hormones in our bodies were at their peak in our late teens: Testosterone, DHEA, Estrogen, Progesterone, Pregnenolone, Dopamine, Vasopressin, Oxytocin, Growth Hormone and Thyroid. High levels of these hormones were responsible for much of the passion as well as the emotional and physical energy of our youth.

Sadly, as we aged, all of our hormone levels began a slow, relentless decline. As these levels dropped, all too often so did our passion for life. At first the more moderate hormone levels of maturity were an advantage: in our late 20′s and early 30′s we still enjoyed great self-confidence and we were very sexually self-aware, but our maturity enabled us to pay attention to the necessary activities of adulthood. That’s why for most people this phase of life, young adulthood, is often the most creative and productive. But as we continued to age and as the hormone levels in our brains and bodies continued to drop, so too did much of our drive, our self-confidence, our zest for life and our physical and emotional resilience.

Usually these emotional and physical declines are slow and imperceptible. Because this decline occurs so gradually, most of us simply adjust our expectations – in spite of an emotional range that may be tending toward depression, and a declining physical capacity, we continue to think we are “normal.” Too often we grow slower, weaker and fatter, until finally we get to the point that we no longer care that we don’t care about much! This process may be normal, but as far as I am concerned, it is not acceptable.

To illustrate this connection between hormone levels and emotional health, consider women in menopause. In their late 40’s and early 50’s, women often undergo a relatively rapid drop in estrogen, testosterone and progesterone. The mood swings, hot flashes, memory difficulties and personality changes associated with this phase of a woman’s life are well known. Tragically, a great number of women in menopause end up on anti-depressants simply because their doctors don’t know how to respond to these symptoms of declining hormone levels. The obvious connection between a woman’s hormone changes and her depression seems to go unrecognized by many physicians.

Some doctors point out that standard hormone replacement therapy for menopausal women seldom relieves the depression. But then, why should it? Traditional hormone replacement therapy does not come close to replacing the hormones that have been lost.  Take estrogen as the most common example. Estrogen is not a “hormone,” but a class of hormones, each with widely differing effects.  The estrogens usually given to women during hormone replacement therapy in the United States are far different from the normal mix of hormones found in healthy, premenopausal women. Astoundingly, for reasons rooted in history rather than science, the usual approach is to recreate in the human woman the normal estrogen balance of a pregnant horse! I’m not making this up. Two thirds of the estrogens found in Premarin, the most commonly used choice in estrogen replacement, are estrogenic hormones found only in horses, donkeys and zebras – never in human beings.

The point I’m making is simple: the best way to recapture the energy and vitality of youth is to rebuild the body’s endocrine support and restore youthful hormone levels. But this process is far more complex than most physicians are prepared to cope with. Using what are called bio-identical hormones – that is, the same hormones normally found in human beings – is a good start. But doing a thorough and effective job requires replacing and balancing all of the hormones found in our youth, not just a few of them. At a minimum, this needs to include Testosterone, Estrogen, Progesterone, Pregnenolone, DHEA, and Thyroid levels. Balancing this complex mix of hormones requires that they be measured and adjusted on a regular basis, because levels in our bodies change constantly, affected by diet, physical activity, emotional and physical stress levels, the amount of fat and muscle in our bodies, and the amount we exercise.

Very few clinics anywhere have the experience and expertise to handle properly all these complex medical challenges like we do at Longevity Medical Clinic. In fact, I cannot think of anyone in the area who has the track record we enjoy at Longevity, successfully treating thousands of patients in the delicate science of proper hormone replacement. If youthful vigor and vitality are the goals you’re seeking, you’re in good, capable and experienced hands at Longevity Medical Clinic.

Because veterinary medicine is less (oppressively) regulated than human medicine, animals are benefiting from stem cell therapies that are safe enough for human use but nonetheless still illegal to commercially develop in the US: “In a very unusual breakthrough, a stem cell treatment for racehorses is ready to be tried … on you. British scientists pioneered a technique in horses where an individuals’ own stem cells are grown outside the body, then injected into the damaged tendon. There will be a clinical trial in the UK in which 24 human patients will undergo this radical new stem cell treatment for similar tendon injuries. We’ll tell you about the proven benefits in racehorses so you’ll understand the possible benefits in people. The test subjects who join the clinical trial will be in the unique position of enjoying a medical procedure that is years behind the veterinary equivalent. If human beings have the same barely believable 80% recovery rate, this will be a leap forward for sports medicine. … The reason animals can get commercial drugs and treatments faster than people in the US and other Western countries is simple: there is enormous oversight in human medical research. Veterinary research is comparably simple. According to the FDA, bringing a new drug to market for humans requires pre-clinical laboratory tests, animal tests, and human clinical trials. Each one of those steps costs money, lots and lots of it. Approval for veterinary drugs is simpler, requiring a single study that proves the drug is safe and effective. Because of regulatory difference, progress on animal medical research can move very quickly compared to human research.”

Link: http://singularityhub.com/2011/03/10/uk-stem-cell-company-cures-race-horse-tendons-humans-next/

Nanotechnology can be used to build assemblies of designed molecules that seek out specific cells – such as cancer cells – but an alternative approach to targeted therapies is to build machinery large enough to be controlled from outside the body, such as the microcarriers demonstrated here: “Soon, drug delivery that precisely targets cancerous cells without exposing the healthy surrounding tissue to the medication’s toxic effects will no longer be an oncologist’s dream but a medical reality … sing a magnetic resonance imaging (MRI) system, [researchers] successfully guided microcarriers loaded with a dose of anti-cancer drug through the bloodstream of a living rabbit, right up to a targeted area in the liver, where the drug was successfully administered. This is a medical first that will help improve chemoembolization, a current treatment for liver cancer. … The therapeutic magnetic microcarriers (TMMCs) [are made] from biodegradable polymer, [measure] 50 micrometers in diameter – just under the breadth of a hair – [and] encapsulate a dose of a therapeutic agent (in this case, doxorubicin) as well as magnetic nanoparticles. Essentially tiny magnets, the nanoparticles are what allow the upgraded MRI system to guide the microcarriers through the blood vessels to the targeted organ. During the experiments, the TMMCs injected into the bloodstream were guided through the hepatic artery to the targeted part of the liver where the drug was progressively released.”

Link: http://www.eurekalert.org/pub_releases/2011-03/pm-wf-031511.php

The Global Forum for Longevity is an industry-sponsored forum taking place later this month; fairly mainstream, no talk of radical life extension or other forms of futurism that might lead to intellectual discomfort for some. I mention it because it is a symptom of the growing interest in biogerontology on the part of the vast insurance industries of the world – which should not be a surprising phenomenon. To find people likely to pay close attention to the future of longevity science, you want to look amongst the folk who stand to gain or lose a great deal of money due to changes in human life spans. Life insurance, pensions, and other forms of making money through managing statistical risks on life expectancy data are, taken together, a very big business indeed.

So here an insurance conglomerate is, as many of them are, sponsoring an event to help spread knowledge through the system: from scientists to actuaries to risk managers and other decision makers in the food chain. Building bridges and forming communities is in and of itself a form of risk management in the long term: it is a way to lower the likelihood of unpleasant surprises by trying to better understand what the scientific community believes are likely outcomes for longevity science over the decades ahead.

Some quotes from the conference site:

We are living in an era of radical change. Longevity offers us all an opportunity to make more ambitious life choices and look to the future with renewed hope. This is why it is vitally important that we move quickly to meet the challenges which it poses for our society.

Drawing on its expertise as an insurer, AXA is playing its part by creating a space to convene an exchange between decision-makers and experts working to ensure this phenomenon is better defined and fully grasped: the Global Forum for Longevity.

…

Our conviction as an insurer and observer of demographic and societal changes worldwide, is that longevity is not a fate to be endured but instead an opportunity. We need to respond quickly in order to meet the challenges which it poses to our society.

“Challenges.” One thing to bear in mind here is that the big insurance groups are inextricably tied in to the unsustainable pension promises made by politicians past and present in many countries around the world – unsustainable even with modest increases in longevity, never mind what is likely to result from the biotechnology revolution. So there is a certain amount of long term public relations work being undertaken by various parties so as to avoid becoming the sacrificial goat in the end when the system of entitlements collapses. You can make your own decision as to how much of the motivation behind this conference falls into that bucket versus the knowledge transfer aims discussed above.

Empires end when an entrenched elite can spend from the public purse and take on debt without immediate consequence or forethought, destroying the value of their currency in the process. Assuming (perhaps optimistically) that present economic empires survive the next couple of decades, a combination of foolish promises and increasing human longevity will be the rock that sinks them.

Are clinical trials using animal studies always valid for humans? Consider me a skeptic.

I frequently see advertisements and newsletters (even some written by physicians) that promote lab tests and treatments based entirely on studies done using rodents. These “experts” frequently draw conclusions from these studies that their lab test or product is a breakthrough of vital importance to humanity. While it may be true, all too often it’s not.

Let me give you a recent example of a study done in mice that could lead to the conclusion that every woman with breast cancer should be taking very robust doses of the adrenal hormone DHEA. This study should serve both as an encouragement and as a caution, an example of the care we must exercise when we use animal studies to draw conclusions about humans.

In this test, laboratory mice had their ovaries removed, and were given a large dose of estrogen each day.  Small pieces of human breast cancer were transferred under the skin of these laboratory mice, and permitted to grow for 9 1/2 months.  During that time, some mice received treatment with DHEA while others did not. At the end of the test period, in the non-DHEA mice the tumors had expanded to nearly ten times their original size.  By contrast, the mice that were given varied doses of DHEA had much smaller tumors.  How much smaller? Depending on the dosage, the tumors in the treated mice were anywhere from 50% to an amazing 80% smaller.  The optimum dose seemed to be about 1 milligram of DHEA daily.

Sounds compelling. But how does this translate into the DHEA dose for a human woman?  Well, let’s do some basic math:

The average laboratory mouse weighs about 20 grams.  I’ll use my wife (with her permission, of course) as a sample female human: she is a small woman, weighing about 50 kilograms (or 50,000 grams). I’m a relatively big guy at about 100 kilograms, or 100,000 grams.  This means that my small wife is about 2,500 times larger than a mouse – and I am about 5,000 times larger!

You can see the obvious problem. Just consider how much DHEA my wife would have to take to match the one milligram mouse dose – 2,500 milligrams of DHEA per day. If I were the patient I would need twice as much: 5,000 milligrams per day!  Since the average over-the-counter DHEA pill provides a 25 milligram dose, my wife would need 100 pills per day and I would have to take 200.

I’ve seen medical studies in which patients were given 100 milligrams per day of DHEA.  The negative side effects were almost nonexistent.  But no one knows what would happen if you gave a human being 2,500 milligrams of DHEA every day, and I frankly don’t know anybody crazy enough to find out. DHEA is a potent participant in the body’s intracrine system (the hormones that work inside our cells). DHEA is converted into a variety of sex hormones in virtually every tissue in the body and is also part of the neurotransmitters within the brain. No one has any idea of what would happen to a human being taking such massive doses.

Does research on rodents and other animals have value? I’m sure it does. But at Longevity Medical Clinic we strongly prefer to base our treatments on peer-reviewed studies done on human beings. That’s a sure way of making sure we’re prescribing just the right dose – for a person, not a mouse!

I notice that Science Progress has thoughtfully posted an overview of a book that, like so many, passed beneath my distracted field of vision. It’s a good overview, and in reading it I’m struck by just how greatly modern fields of intellectual study have devolved into the title of this post – efforts to find smart ways to say profoundly stupid things. This isn’t the aim and goal at the outset, of course, but with postmodernism leading the way, there is a well defined sort of style that accompanies the ability of a community of intellectuals to cut themselves off from rationality and evidence in order to build castles in the sky. Up becomes down and left becomes right, and all sorts of nonsense rises to rule the roost. The end result is a core of stupidity well wrapped by a tremendous expenditure of earnest intellectual effort: a sort of Emperor’s new clothes situation wherein few parties involved have any incentive to point out the obvious.

Outside of theology and the worst reaches of postmodernism, this disconnect from reality is perhaps most evident in modern macroeconomics – largely an effort to convince the world against all the evidence that up is down and black is white – and the various fields of ethics, such as bioethics. The bioethics community in particular long ago lost its way.

But back to some examples from that Science Progress piece:

When I say that here, too, Agar builds his argument on an appeal to nature, I have in mind his foundational premise regarding what he calls “species relativism.” The “relativism” part of that label might at first sound like a rejection of anything resembling an appeal to nature. But Agar holds that there is something good, something worth preserving, about the way members of our species typically or naturally find happiness. As he puts it, “Experiences typical of the ways in which humans live and love are the particular focus of my species-relativism” (pg.15).

So for an enhancement to count as moderate on Agar’s account, it has to be “relative” to our species. As distinct from a radical or “purported” enhancement, a moderate one has to enhance a way of being that is typical of homo sapiens.

…

He argues that, while it is indeed reasonable to want more of “a recognizably human life,” it is not reasonable to want a form of life without the sorts of experiences that are typical for members of our species. As he says, there are some Galapagos tortoises that live up to 150 years, and they no doubt enjoy experiences that are pleasurable for members of their species, but no human being would trade our “distinctively human varieties of pleasure” for distinctively tortoise varieties of pleasure. Because, however, he grants the respect in which that example is unfair – becoming a tortoise would entail diminished cognition and radical life extension would not – he needs to say more.

He begins by suggesting that de Grey’s “Strategies for Engineered Negligible Senescence” (SENS) might create an obsessive fear of death, which might come to completely dominate the lives of those who adopted such strategies. Agar worries that, because negligibly senescent people would have more years of life to lose if they failed in one of their projects, they would have a strong reason not to take any risks at all (pg. 116). Indeed, at this point he invokes the concern that later in the book he will call its central theme: the concern about alienation, about becoming separated from the kinds of, here, risky experiences that constitute human lives as we know them. According to Agar, de Grey’s ambition to radically extend our lives “is likely to alienate us from the things and people who currently give our lives meaning” (pg. 122).

Agar allows that there may appear to be a way around the obsessive fear of death that SENS could bring about. To get around the risks associated with going out into the real world, he allows, negligibly senescent people could use technologies to have virtual experiences instead. But the problem with that strategy, he says, is that it fails to appreciate the extent to which human beings want “direct” contact with the “real” world. It fails to appreciate that “We think differently about these kinds of indirect contact [with the real world] than we do about ‘being there.’” No one, he suggests, thinks that “seeing a Discovery Channel documentary filmed on Mount Everest substitutes for actually climbing it” (pg. 123).

Castles in the sky, and straw ones at that. I would hope that little needs to be said in response to this sort of thing – it is so self-evidently hollow, a gut feel trying to cover itself in words and failing, that it falls apart at a glance.

A study published in the February issue of the Chest revealed that vitamin D deficiency is linked to a higher risk of interstitial lung disease.

The Lungs

The principal function of the lungs is to transport the oxygen acquired through breathing to the blood streams and to release carbon dioxide back to the atmosphere. The whole process of respiration is accomplished by tiny specialized cells called alveoli or the air sacs. In the process of breathing, air passes through the nose then travels through the nasopharynx, larynx, trachea and through the branches of the bronchial tubes before finally reaching the aveoli. The diaphragm, on the other hand, is important in driving air to the lungs.

Pulmonary Health Risks

The increasingly deteriorating conditions of the environment make it even harder to keep the lungs healthy. Though the lungs are naturally capable of filtering the air that we breathe, they may not be able to filter toxic materials in the air that may affect our health. This results to lung problems that can be life threatening. Lung cancer, for example, has a high prevalence rate in the United States and other parts of the world.

The number one cause of lung damage is smoking. Numerous studies had found out that smoking can dramatically increase the risk of developing lung cancer and other pulmonary disorders. A single stick of cigarette can contain hundreds of toxins and harmful materials that can directly harm the lungs and other vital organs of the body. Indeed, smoking is bad for the health. Other factors and bad habits can also result to an increased risk of developing lung disease. Inhaling aerosols like paint and deodorants can result to serious damage of the lungs. Vehicles like trucks and cars release toxic fumes that can damage the lungs when inhaled. The lack of sufficient nutrition can also lead to certain lung problems.  A study published in the February issue of the Chest revealed that vitamin D deficiency can increase the risk of interstitial lung disease, a health condition associated with inflammation of the tissues surrounding the air sacs.

Interstitial Lung Disease

The air sacs found in the inner lining of the lungs plays a very important role in extracting oxygen from the air and are supported by a thin lining of tissue. When this tissue becomes inflamed, the function of the air sacs is affected. This health condition of the lungs is called interstitial lung disease. ILD is not limited to certain portions of the lungs but the inflammation can spread all throughout the lungs. Unlike pneumonia, the inflammation of the lungs in interstitial lung disease is not caused by infection but by other factors including the misdirected response of the immune system to infection and toxins like silica dusts and asbestos. Other cases of ILD are idiopathic or with no definite cause.

The first symptom of ILD is difficulty in breathing due to the reduced amounts of circulating oxygen in the body followed by frequent coughing. The condition can be mistakenly diagnosed as pneumonia. Health examinations to conclude ILD include blood tests to rule out infection, imaging studies like CT scans and chest x-rays, PFT or pulmonary function tests and biopsy. Though all these tests are not required in order to determine ILD, some cases may need more examinations that others.

Vitamin D Deficiency and Lung Health

In a study conducted by a team of researchers from the University of Cincinnati College of Medicine, results revealed that vitamin D deficiency can affect the proper function of the lungs. The researchers observed that patients with interstitial lung disease or ILD are mostly deficient in vitamin D especially in patients with connective tissue disease or CTD. They gathered a group of 67 patients with CTD-ILD and 51 patients with other types of ILD and found that the prevalence of vitamin D insufficiency and deficiency is 69 percent and 38 percent, respectively.  Vitamin D plays an important role in maintaining healthy lung function. And aside from keeping the respiratory system in tip-top shape, vitamin D also plays an essential role in other body functions.

Health Benefits of Vitamin D

United States laws require the fortification of all milk brands with vitamin D. So drinking one to two glasses of milk a day can supply the body with its needed dosage of vitamin D to maintain and promote better health. Other rich sources of vitamin D are cream, butter, and other dairy products. Some oysters and fish are also rich sources of vitamin D.

The efficient absorption of calcium in the bones need the assistance of vitamin D. Vitamin D deficiency is commonly associated with rickets in children and osteoporosis in older adults. Too much vitamin D can also have adverse effects to the body since it results to the excessive absorption of calcium which can accumulate in vital organs like the heart and lungs. Muscle weakness, vomiting and the appearance of kidney stones are also linked to too much vitamin D.

Infants and children aged 0 to 13 years need 5 micrograms of vitamin D a day; this recommended daily intake of vitamin D is relatively consistent up to the age of 50 with an increase to 10 micrograms for people 51 years and older.

Natural Ways to Promote Lung Health

Frequent exercise, proper nutrition and avoiding harmful habits are keys to keeping the lungs healthy. Even if the person exercise frequently and is receiving sufficient nutrition, smoking can keep his risk of developing lung disease high compared to sedentary and malnourished non-smokers. It has been well established that smoking can lead to numerous health conditions like lung cancer and other types of cancer. Smoking can also weaken the immune system and make the person more susceptible to infection.

Medical experts advise regular check-ups for the early diagnosis of a lung disorder. Taking the stairs instead of using the lift will also give the lungs a healthy workout if there’s no time to go to the gym. Second hand smoke can damage the lungs more than cigarette does to the actual smoker. So try to stay away from smoky areas and always make it a point to take the non-smokers area in bars and restaurants. Certain household products may also release toxic fumes when used. Make it a habit to always check the labels of household cleaning products before buying or using them.

Sources
medicinenet.com
eurekalert.org
medicinenet.com
nlm.nih.gov
ods.od.nih.gov
rd.com

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A study conducted by a team of researchers from the University of Lausanne found that a diet rich in whey protein can reduce the amount of fat in the liver.

Researchers from the University of Lausanne found out that the supplementation of whey protein in a person’s diet can lower the risk of developing fatty liver disease in obese women by reducing the amount of fat in liver cells. The study was published in an issue of Clinical Nutrition. They also found that whey protein was able to improve the study participants’ blood lipid profile which is important in promoting a healthier heart. The participants were asked to take the whey protein supplements for a period of four weeks.

Lead researcher Murielle Bortolotti said that their study was uncontrolled and preliminary but it strongly suggests that whey protein supplementation helps reduce the risk of fatty liver disease and promotes cardiovascular health as a long-term benefit. The researchers gathered a group of obese patients with an average BMI of 37.6 and IHCL concentrations between 1.9 to 20.5 percent. The participants were also recorded to have noticeable resistance to insulin with an average insulin sensitivity score of 2.77. The researchers observed that, after four weeks of whey protein supplementation, the study participants’ average IHCL dropped by 21 percent while their plasma triglyceride levels also went down by 15 percent. Their overall plasma cholesterol concentration was down by more than 7 percent after about a month of taking whey protein supplements. Researchers said that the result of the study indicates that whey protein has the potential to improve triglyceride profiles and IHCL.

The Liver and Fatty Liver Disease

The liver is the largest and heaviest glandular organ in the human body with an average weight of 1.36 kilograms. It is divided into four lobes which are unequal in size and shape. It is located at the right part of the abdominal cavity and just below the diaphragm. The portal vein and hepatic artery are responsible for carrying nutrients from the small intestines and oxygen-rich blood to the liver, respectively.

The human liver serves numerous functions including the production of enzymes that break down fats and produce glycogen from glucose. It is also responsible for producing urea and certain amino acids, storing of vitamins like vitamins B12, K, D, A and some minerals. The liver also produces 80 percent of the cholesterol in the body. The common disorders of the liver are liver cirrhosis, liver cancer, hepatitis and Wilson’s disease. The most harmful habit that affects the proper function of the liver is the excessive drinking of alcohol which can potentially alter the metabolic processes in the organ.

The root cause of fatty liver disease remains to be unknown. But medical experts are looking at patients’ resistance to insulin as the primary cause of the condition. Insulin resistance is a metabolic disorder where the cells are no longer responding properly to insulin in order to metabolize glucose.  In other words, insulin is no longer capable of performing its natural task of regulating sugar levels in the body. Nonalcoholic fatty liver disease is characterized by the accumulation of fat in the liver without the presence of alcohol. It refers to a wide spectrum of liver diseases from steatosis or simple fatty liver, cirrhosis or the irreversible and advanced scarring of the liver, to nonalcoholic steatohepatitis. Fatty liver disease is common throughout any age group; children can start developing fatty liver disease at the age of 10.

Natural Ways to Promote Liver Health

The liver is a very important organ in the body. Though minor health conditions concerning the liver are often very treatable, it is still necessary to keep the liver functioning properly to promote overall health.

• Diet plays a very important role in keeping the liver in tiptop shape. Ignoring hunger pangs or sudden and unscheduled eating can literally surprise the liver. Every time this happens, the liver exerts effort to produce the necessary enzymes to digest and metabolize the food properly. Eating at different hours of the day will overwork the liver and cause it to become exhausted. When struck with a sudden desire to eat, choosing foods that are not too heavy to the stomach like salads and fruits is recommended. And it is also a good way of maintaining a healthy body weight.

• Drinking plenty of water helps in washing away impurities and toxins out of the kidneys and liver. But drinking too much water while eating can interrupt the normal digestive process. So remember to observe proper pacing.

• The body has a limited requirement for sugars. Eating too much sweet foods can be dangerous to the liver and the human body. Sweets, especially those made or composed of refined sugar, will result to the excessive accumulation of fats in certain body parts like the buttocks, abdomen, thighs and the liver. Too much refined sugar will also result to the production of more triglycerides in the blood which, in turn, can increase the risk of developing cardiovascular disease. Some artificial sweeteners had been found by different studies to be poisonous to the body and result to fatigue and hypoglycemia. Eating fruits or blackstrap molasses when you want to eat something sweet are excellent alternatives to artificial sweeteners, especially for individuals with diabetes.

• Foods rich in protein like eggs, chicken, whole grains and legumes can help promote better liver health by helping it maintain a normal protein level in the body since the liver is responsible for producing protein. Low levels of protein can be a strong indication of kidney and liver disease. Eating natural and organic foods that are free of artificial sweeteners, colors, flavors and preservatives can also help in keeping the liver healthy.

• Some disease-causing bacteria can breed in the intestines. These organisms can cause permanent damage to the liver. So it is important to keep the intestines clean by drinking enough liquids and foods rich in dietary fiber.

• Eating less to lose weight can result to an insufficiency of nutrients supplied to the body. This makes the liver weak and incapable of producing enzymes that are needed in the proper digestion of food. Stop worrying too much about gaining weight and instead direct your attention to the foods that you eat to keep your liver and body healthy. As a reward, your liver will be able to better digest food and contribute in managing your weight.

Sources
nutraingredients.com
gicare.com
medicinenet.com
fitness.ygoy.com

Discuss this post in Frank Mangano’s forum!

At Longevity Medical Clinic we often talk to our patients about detecting and preventing cancer. It’s something on the minds of most of us, since we all know that, when it comes to treating cancer, early detecting is critical. One of my patients recently asked me about they had read concerning an early detection test for cancer. Are these tests valid, or do they offer a false hope?

In fact, thanks to advances in early detection, there are now some promising tests for cancer. These tests look for what we call “markers” – early signs of cancer.  But the fact is that each cancer has its own specific set of markers, sometimes as many as 30 or 40 that doctors can actually measure. In many cases, in order to get an early detection test that is statistically valid, doctors need to combine 15 or 20 of these markers. You can see how complicated this can get.

Let’s consider one specific example – lung cancer. Almost 5 years ago, medical journals began reporting on the first early detection tests for this dreaded form of cancer. Since 2006 this test has been “fast-tracked” by several different biotech firms, each working to refine this test which looks at six different cancer-related antigens. In terms of sensitivity, this new test is a bit less sensitive than a CT scan; however, the good news is that it can detect tumors that are smaller, and also cancers that are less advanced, giving doctors a head start on treatment options. The new test, called CDT, is also more specific.

But we need to put this into perspective. When doctors perform a CT scan and find a small nodule in the lung, only about 3% will turn out to be cancerous. By contrast, with the newer CDT test, about 10% of the nodules will be cancerous. So the CDT test is indeed a major step forward for accuracy. On the other hand, 90% of CDT-tested patients with suspicious nodules in the lung will turn out to be cancer-free, something they only find out after expensive and invasive lung biopsies.  Some wonder whether this downside, not to mention the fear that comes from waiting for the biopsy results, is worth it. At present this newer CDT test is only being performed on patients at high risk for lung cancer, particularly heavy smokers.

So what’s the conclusion? Well, the fact is that this CDT test is a long way from perfect. However, right now it is the best tool we have available to diagnose early lung cancer in high risk patients.  If you’re wondering about these or other cancer tests, please talk with the staff here at Longevity Medical Clinic on your next visit.

From ScienceDaily: “It has been long known that stress plays a part not just in the graying of hair but in hair loss as well. … Now, a team [that] was investigating how stress affects gastrointestinal function may have found a chemical compound that induces hair growth by blocking a stress-related hormone associated with hair loss – entirely by accident. … Our findings show that a short-duration treatment with this compound causes an astounding long-term hair regrowth in chronically stressed mutant mice. This could open new venues to treat hair loss in humans through the modulation of the stress hormone receptors, particularly hair loss related to chronic stress and aging. … the researchers had been using mice that were genetically altered to overproduce a stress hormone called corticotrophin-releasing factor, or CRF. As these mice age, they lose hair and eventually become bald on their backs, making them visually distinct from their unaltered counterparts. The [researchers] had developed the chemical compound, a peptide called astressin-B, and described its ability to block the action of CRF. … researchers injected the astressin-B into the bald mice to observe how its CRF-blocking ability affected gastrointestinal tract function. …. About three months later, the investigators returned to these mice to conduct further gastrointestinal studies and found they couldn’t distinguish them from their unaltered brethren. They had regrown hair on their previously bald backs.”

Link: http://www.sciencedaily.com/releases/2011/02/110216185406.htm

The investigation of the mechanisms of calorie restriction continues apace. Here, researchers “report for the first time that deactivation of a protein called CRTC1 in roundworms increases their lifespan, most likely mediating the effects of calorie restriction. Previously, researchers knew hunger promoted longevity by activating an enzyme called AMPK, which senses that food is scarce and pushes cells into a low energy state. … We knew AMPK was a major energy sensor but didn’t know what it was talking to. Our goal was to understand the genetic circuitry that registered that response. … It was clear that one pathway that coordinated metabolism with growth in response to nutrients was AMPK signaling. Studies had also suggested that AMPK might regulate lifespan in worms. What was not known was what factors downstream of AMPK mediated those effects. … they searched the genome of Caenorhabditis elegans for likely AMPK targets, and identified one suspect encoding a protein called CRTC1, which was expressed at the same time and place as AMPK. To determine if CRTC1 played any role in lifespan, the team fed worms an inhibitory RNA engineered to deplete them of CRTC1 protein. When they measured the worms’ lifespan-normally about 3 weeks-they found that worms fed the anti-CRTC1 RNA lived a whopping 40% longer, suggesting that AMPK retards aging by antagonizing CRTC1 activity. … AMPK deactivated CRTC1 by adding phosphates to a specific region of the CRTC1 protein, an effect equivalent to eliminating CRTC1 altogether. Likewise, when the worms were fed an inhibitory RNA depleting them of an enzyme that lops off the CRTC1 phosphates, they lived longer, showing that AMPK and the lopper – known to scientists as calcineurin – determine lifespan by controlling the extent to which CRTC1 is phosphorylated.”

Link: http://www.newswise.com/articles/hungering-for-longevity-salk-scientists-identify-the-confluence-of-aging-signals

Around these parts Aubrey de Grey and the SENS Foundation should require no introduction. His advocacy and the Foundation’s work on the science of repairing aging is well known, and has been mentioned here at Fight Aging! too many times to count. In my eyes, the Strategies for Engineered Negligible Senescence (SENS) continue to be the best extant plan for extending human life span as rapidly as possible – and within our lifetimes. The more funding that is devoted to realizing that plan, the better all of our futures will be.

I noticed that a podcast interview with de Grey is up at the Singularity Weblog:

Last time I had Dr. Aubrey de Grey on Singularity 1 on 1 the interview turned out to be a hit. In fact it is still by far the most popular podcast that I have done and the audio file has been listened to or downloaded over 30,000 times. Given Aubrey’s popular appeal and the importance of his work, it is no surprise that I am very happy to have him back for a second interview. … During this conversation I ask Dr. de Grey to discuss issues such as: the term natural death and its impact; the publicity and importance of two long-awaited documentaries about Ray Kurzweil – Transcendent Man and The Singularity is Near; traditional metabolic and more recent DNA tests such as the ones done by 23andMe and others; the slow developmental process of new drugs and therapies, and the problems of taking them from testing in lab rats to humans; the Thomas Malthus argument of overpopulation and Aubrey’s reply to it.

Head on over there to watch or listen.

From the Monterey Herald: ” Within a Northeast Ohio lab, a hairless mouse is growing an ear from the cells of a Wadsworth, Ohio, preschooler. Dr. William Landis, the G. Stafford Whitby Chair of Polymer Science at the University of Akron, is leading groundbreaking, tissue-engineering research to grow human cartilage – first in the lab, now in animals and, eventually, in patients. His work is part of a fast-developing field that could help millions of patients repair injuries, replace worn body parts or fix birth defects with tissue grown from their own cells in the not-so-distant future. … Kyle Figuray’s parents agreed to be the first area participants and donors of his otherwise useless cartilage. The healthy, friendly 5-year-old was born with a congenital defect that caused the exterior ear and ear canal on his right side to develop improperly. Typically, the malformed ear cartilage is discarded as medical waste after it’s removed during the first of three procedures to craft a new ear out of rib. Instead, the tissue removed [was] placed inside a vial and shared with Landis’ research team, who carefully cleansed the cells and fed them special nutrients to coax them to proliferate in the lab. A few weeks later, enough cells were available for researchers to ’seed’ them onto a biodegradable, biocompatible polymer scaffold. A few days later, the seeded ear scaffold was implanted under the skin of a hairless mouse … The mouse will be studied over the next year to determine how the cells are behaving and progressing toward normal cartilage. If all goes well, the biodegradable polymer scaffold should disappear, leaving behind only Kyle’s cartilage cells in the shape of an ear. The hope is that an affected person’s cells someday can be harvested, seeded onto similar polymer scaffolds and implanted under the patient’s own skin in the abdomen or back until they grow into replacement tissue. At that point, the new tissue could be removed and used to replace the patient’s injured or defective tissue.”

Link: http://www.montereyherald.com/science/ci_17411698

The latest issue of Rejuvenation Research is available online, and it opens with what is perhaps one of the best of points to make in a world in which people are dying all around us:

I welcome Dr. Paula Moreira as a new member of our editorial board, but for the worst possible reason. Moreira has been appointed as a replacement for Mark Smith, a fellow professor at Case Western Reserve University, who tragically died in a car accident late last year. What is even worse is that Smith is not the only loss that the field of biogerontology has suffered in 2010. In fact, I am aware of fully five other researchers who died during 2010. Amir Abramovich (whose Ph.D. advisor has penned a brief obituary that appears later in this issue) and Estela Medrano also succumbed to road accidents. James Joseph died from complications following heart surgery. Chris Heward was the victim of a particularly aggressive esophageal cancer. And Bob Butler died very suddenly of leukemia.

…

I have chosen to highlight these sombre events in this space not only to commemorate lost friends and colleagues. My main reason for doing so is to draw attention to the questionable validity of our tendency to grieve especially intensely for those who die when still highly active. Though I share this tendency, I think it deserves scrutiny, because it is founded on an assumption that profoundly contradicts the motivation for the work to which we, as did the colleagues I have just listed, dedicate our lives.

Aging kills people, just as cars do. There are only two things that distinguish aging from other killers: it kills people very slowly, only after gradually and progressively debilitating them over many years, and it only kills people who were born quite a long time ago. The combination of these features seems to be the only available explanation for why we so meekly and calmly accept the deaths of so vast a number of people from aging, while feeling much more intense anger and despair at the comparatively rare deaths that occur in the industrialized world at younger ages.

…

Is it somehow OK, or at least only a little bit sad, when someone dies of “natural causes” after “a good innings”? I would suggest that it is not OK.

Ageism permeates our societies, and our descendants will look back in disgust and horror at the way in which we allowed our historical legacy of prejudice to suppress and slow down progress towards the biotechnologies of rejuvenation. We younger folk write off the old in so many ways, and in doing so each of us is only sticking the knife into the person we’ll be a few decades down the line – and teaching our children to do exactly the same. Every death is a tragedy, but so many people work so hard to pretend otherwise.

Old people suffer from a terrible debilitating medical condition: aging. Why view them any differently than the victims of any other deadly disease? If not weighed down by the degenerations of aging and the knowledge of suffering a certainly terminal condition, elderly folk could contribute greatly to all fields of human endeavor, applying the experience and knowledge of a lifetime – or adeptly applying the savings of a lifetime to fund the work of others. We would all be far wealthier if the ongoing ability to create value offered by human beings was not destroyed after a bare few decades of productivity.

Even if it wasn’t the case that it is in our immediate economic self-interest to build rejuvenation biotechnologies, working to cure aging would still be the greatest of charitable causes. No other aspect of human biology or the human condition causes as much pain and death.

Aging is a horror, and it twists our society into further horrors – such as the often shameful ways in which the young treat the old. The sooner that aging can be repaired and removed as a threat to human existence, the better the human condition will become.

A promising open access study: “Transplanting autologous renal progenitor cells (RPCs), (kidney stem cells derived from self-donors), into rat models with kidney damage from pyelonephritis – a type of urinary infection that has reached the kidney – has been found to improve kidney structure and function. … Advancements in stem cell therapies and tissue engineering hold great promise for regenerative nephrology. Our RPC transplant study demonstrated benefits for pyelonephritis, a disease characterized by severe inflammation, renal function impairment and eventual scarring, and which remains a major cause of end-stage-renal disease worldwide. … The researchers divided 27 rats into three groups, two of which were modeled with an induced pyelonephritis in their right kidneys, while the third group did not have induced disease. RPCs were obtained from the diseased animals’ left kidneys and injected into the right kidney six weeks later. Two weeks after injection, tubular atrophy was reduced. After four weeks, fibrosis was reduced and after sixty days, right renal tissue integrity was ’significantly improved.’ … We propose that kidney augmentation was mainly due to functional tissue regeneration following cellular transplantation. Kidney-specific stem/progenitor cells might be the most appropriate candidates for transplantation because of their inherent organ-specific differentiation and their capacity to modulate tissue remodeling in chronic nephropathies. … The researchers concluded that because renal fibrosis is a common and ultimate pathway leading to end-stage renal disease, amelioration of fibrosis might be of major clinical relevance.”

Link: http://www.eurekalert.org/pub_releases/2011-02/ctco-sct021411.php

There is clearly a point in Alzheimer’s, and other neurodegenerative diseases, beyond which the damage caused by the condition is irreversible. Neurons die, and in large enough numbers to destroy vast swathes of information held in the brain – the very foundation of who you are, and the vital components of systems needed to live a normal life. All is not gloom, however. Studies in past years have suggested that up to that point, much of the loss of function that accompanies Alzheimers is in principle reversible:

Some evidence suggests that the worst effects of Alzheimer’s disease can be repaired – that memories are not destroyed, but rather become inaccessible.

Another recent study adds to this picture:

Amyloid-beta and tau protein deposits in the brain are characteristic features of Alzheimer disease. The effect on the hippocampus, the area of the brain that plays a central role in learning and memory, is particularly severe. However, it appears that the toxic effect of tau protein is largely eliminated when the corresponding tau gene is switched off.

Researchers from the Max Planck Research Unit for Structural Molecular Biology at DESY in Hamburg have succeeded in demonstrating that once the gene is deactivated, mice with a human tau gene, which previously presented symptoms of dementia, regain their ability to learn and remember, and that the synapses of the mice also reappear in part. The scientists are now testing active substances to prevent the formation of tau deposits in mice. This may help to reverse memory loss in the early stages of Alzheimer disease – in part, at least.

For yet another consideration of early to mid-stage Alzheimer’s as a form of dynamic blockage of memory access, you might also look at the effects of some newer anti-inflammatory treatments:

The [study from 2008] documents a dramatic and unprecedented therapeutic effect in an Alzheimer’s patient: improvement within minutes following delivery of perispinal etanercept, which is etanercept given by injection in the spine.

Putting aside a discussion of the mechanisms by which this happens, the very fact that it can happen demonstrates the possibility of reversing the worst aspects of Alzheimer’s. Thus memories and the working structures of the brain must remain largely intact until fairly late in the progression of the disease.

Research into Laron dwarfism in a population in Ecuador has been taking place for a few years now: “People living in remote villages in Ecuador have a mutation that some biologists say may throw light on human longevity and ways to increase it. The villagers are very small, generally less than three and a half feet tall, and have a rare condition known as Laron syndrome or Laron-type dwarfism. … though cancer was frequent among people who did not have the Laron mutation, those who did have it almost never got cancer. And they never developed diabetes, even though many were obese, which often brings on the condition. … [this is] an opportunity to explore in people the genetic mutations that researchers [found] could make laboratory animals live much longer than usual. … The Laron patients’ mutation means that their growth hormone receptor lacks the last eight units of its exterior region, so it cannot react to growth hormone. In normal children, growth hormone makes the cells of the liver churn out another hormone, called insulinlike growth factor, or IGF-1, and this hormone makes the children grow. If the Laron patients are given doses of IGF-1 before puberty, they can grow to fairly normal height. This is where the physiology of the Laron patients links up with the longevity studies that researchers have been pursuing with laboratory animals. IGF-1 is part of an ancient signaling pathway that exists in the laboratory roundworm as well as in people. The gene that makes the receptor for IGF-1 in the roundworm is called DAF-2. And worms in which this gene is knocked out live twice as long as normal.”

Link: http://www.nytimes.com/2011/02/17/science/17longevity.html

The Science for Life Extension Foundation is a Russian organization consisting of advocates and aging researchers. They are similar to the SENS Foundation in that they undertake a mix of fundraising, directing research, organizing events, advocacy for longevity science, and publishing on potential methodologies to extend the healthy human life span. These two groups even share some members and advisors in common – it’s a small world these days, after all, and aging research is not a large community to begin with. That is one of many things we like to see change over the next decade or two: if you want rapid progress, there need to be many researchers at work.

The Science for Life Extension Foundation has published a number of professional quality documents that can be downloaded in PDF format from their website. Unfortunately not all of them are available in English, and automated translation of PDFs remains somewhat hit and miss. I did want to direct your attention to one of the documents, however, which is entitled “25 Scientific Ideas of Life Extension.” It is a very elegantly designed, very clear booklet aimed at investors. The PDF packages up a series of scientific research programs aimed at extending human life into compelling elevator pitches – but just saying that doesn’t do it justice. It really is very well done indeed, and you should take a look:

I picked out one of the twenty-five that focuses on a research theme you might be familiar with, as I’ve mentioned it in the past. If you look back in the Fight Aging! archives, you can read more about Cuervo’s work on autophagy and lysosomal receptors:

• A Little More On Preventing Decline in Liver Function With Age
• An Update on Cuervo’s Autophagy Research

In experiments, livers in genetically modified mice 22 to 26 months old, the equivalent of octogenarians in human years, cleaned blood as efficiently as those in animals a quarter their age. By contrast, the livers of normal mice in a control group began to fail. … While her paper does not show increased survival rates among the mice, le Couteur, who has advised her recently on the research, says Cuervo does have data on improved survival rates which she intends to publish.