Category Archives: Longevity Medicine

A study revealed that anthocyanins found in berries can help lower blood pressure and thus, manage hypertension.

Hypertension is otherwise known as high blood pressure or tensing of the arteries due to high pressure build-up. These arteries enable the transportation of blood from the heart to all the major organs and tissues in our body.  There are multiple causes of hypertension, such as obesity, chronic renal failure, diabetes mellitus type 2, renal infarction and even pregnancy. The normal blood pressure is within the bounds of 120/80, blood pressure ranging to 139/89 is categorized as pre-hypertension, and blood pressure of 140/90 and above is placed on the high category.

Symptoms of hypertension includes chronic headaches that goes on for days, vertigo or dizziness, nausea, heart palpitations, double vision or blurry, drowsiness, general fatigue, shortness of breath, and buzzing in the ears commonly known as tinnitus.

Hypertension Management

A treatment for this specific ailment varies but the most efficient cure for hypertension is using a complex approach. It includes patient’s history, age, gravity of the condition, therapy schemes that will concentrate on the ailment’s precise cause. Hypertension curable and it all begins with prevention.  This consists of keeping a healthy weight and lifestyle by avoiding excessive intake of alcohol, smoking cessation, and eating a well-balanced diet and regular exercise. Long ago, hypertension can only be controlled through the use of medications – but not anymore.

More natural forms of treatments are currently being introduced in the market. A study indicates that anthocyanins, a type of flavonoid found in strawberries, blueberries, cherries, purple grapes as well as in vegetables such as purple cabbage and beets, is helpful in alleviating high blood pressure.  According to a research study done by scientists from the Harvard School of Public Health, Harvard Medical School and a UK based University of Anglia, multiple intake of anthocyanins reduces the dangers of hypertension by up to 12 percent. Hence, the most important advantage one can get from taking in foods that are rich in anthocyanin is the management of hypertension. Cardiovascular diseases (CVD) are a result of chronic hypertension, and it is known to causes half of Europe’s death, and at the same time tallying Europe’s economy expense around $202 billion per year.

Research Findings

For an average span of 14 years, Harvard’s Eric Rimm led the researchers in gathering data from various subjects, consisting of 133, 914 women, and 23,043 men. Flavonoids and other subcategories were analyzed using questionnaires regarding food frequencies and were distributed every 4 years. An accumulation of 5,629 and 29,018 documented cases of hypertension were tabulated in men and women, correspondingly.

When the figures were finally reported, the researchers discovered that the topmost average consumption that ranges from 16.2 to 12.0 milligrams daily was correlated to an 8 percent reduction to the dangers of hypertension. On the other hand, a 12 percent increase in lowering hypertension risk was tabulated among subjects with ages from 60 and above, as compared to the nethermost consumption of anthocyanins, ranging from 5.7 to 6.8.

While no other subcategories of flavonoids were related to high blood pressure, researchers however, observed that the compound apeginin was linked to a 5 percent decrease in risk. When the maximum and minimum levels of intakes were compared, researchers added that a 6 percent reduction in the dangers of hypertension was noted for subjects over the age of 60 that has the topmost average consumption of flavan-3-ol catechin.  Also an important finding was documented stating that the consumption of blueberries among people of the same age group lessened their risk of hypertension by up to 10 percent compared to those who did not consume any blueberries. Dr. Rimm and his colleagues wrote that the results reinforce the theory that antihypertensive biological activities may be applicable to the processes of vasodilation linked with a particular flavonoid physical attribute.

Key Elements

According to Dr. Rimm and his colleagues, there is an existence of vast flavonoid structural varieties, but the likelihood that it can lower the effects of blood pressure is inadequate with regards to its similar anatomical composites which include the catechol and 4’ hydroxy flavonoids.

In addition, the research findings implies that distinct categories of flavonoids are connected with lowering blood pressure especially anthocyanins.  The data is highly significant due to the fact that anthocyanins are commonly found in blueberries, strawberries, cranberries, fruits that are normally consumed and can be easily added to a person’s dietary needs. Researchers also added that blackcurrants, blood orange juice and blueberries have an additional 500 mg of anthocyanins.

The researchers added, that the fundamental biological process wherein flavonoids helps control blood pressure comprise the influence of flavonoids with regards to the vascular movement of blood, vascular reactivity, and the process of glucose uptake.

However, researchers from the American Journal of Clinical Nutrition states that the research needs additional thorough investigations, which will include intervention analysis to assess the ideal dosage of foods that are rich in anthocyanin that could prevent hypertension and reinforce the recommendation and remedy of hypertension.

Additional Information Regarding Flavonoids

Other than hypertension, anthocyanin, the flavonoid compound is also recognized by countless laboratory researches.

• Based on findings, anthocyanin is also potent in preventing cancer by delaying the development of pre-malignant cells, hastening apoptosis, which effectively kills cancer cells in a faster rate.
• It also helps in controlling inflammation by dampening allergic reactions.
• It also cancels out enzymes that damage the connective tissue and its antioxidant properties blocks oxidants from destroying connective tissue.  Furthermore, it repairs proteins that were damaged in the blood vessel wall.
• Anthocyanins, at the same time hinders abnormal protein production, a significant importance for diabetic patients, since profuse protein production may lead to retinopathy which takes place when the body tries to repair leaks from damage capillaries.
• Lastly, anthocyanins may help prevent brain damage. Since the human brain is highly vulnerable to damage by peroxynitrite nitration of tyrosine excess in proteins and enzymes causing neurodegenerative ailments and possible brain trauma. The nitrates impede receptor sites, hence stopping neural growth and restorative processes.  Anthocyanins’ job is to aid the brain by protecting it against neurological diseases.

Sources
madsci.org
medicinenet.com
nutraingredients.com
chiro.org
wrongdiagnosis.com
symptoms-of-hypertension.com
en.wikipedia.org

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There's always something interesting in the news when it comes to progress in regenerative medicine and tissue engineering. This is the sort of research community we want to see for every field that might impact human aging and longevity: large, thriving, dynamic, and attracting plenty of attention and funding. The practical result is that we live in exciting times - organ regrowth is right around the corner, as is the prospect of meaningful repair or replacement of many types of aged tissue. Regenerative medicine is not a one-stop solution for all of aging, but it is one of the necessary pillars of the true rejuvenation biotechnology that will be developed in the decades to come.

Here are a few articles that caught my eye of late; the mainstream media seems to be picking up the level of attention they are giving to the cutting edge of regenerative medicine these days.

Seeing local scientists at heart of regenerative medicine

In one lab, a surgeon builds a pink, pulsing heart, cell by cell. In another, a researcher literally sprays new skin onto severely burned patients. Elsewhere, a scientist re-creates the delicate folds of the ear - on the back of a mouse. Sound like science fiction? It already is science: Researchers in Boston and beyond are building everything from blood vessels to internal organs, using engineering tricks and dome-like bioreactors. Tonight, in 'How to Build a Beating Heart,' National Geographic Explorer investigates those efforts to transform human health, revealing the pulse-quickeningly cool side of regenerative medicine.

Building body parts: Saving lives, salamander style

If an injured salamander can grow a new limb, why can't a human? Maybe they can, say researchers at the Armed Forces Institute of Regenerative Medicine. Starting with stem cells from patient's bodies, scientists at this Wake Forest University facility have grown 22 different types of tissues and organs. Lives are being saved and more amazing successes are on the way.

Skin cells help to develop possible heart defect treatment in first-of-its-kind Stanford study

Using skin cells from young patients who have a severe genetic heart defect, Stanford University School of Medicine scientists have generated beating heart cells that carry the same genetic mutation. The newly created human heart cells - cardiomyocytes - allowed the researchers for the first time to examine and characterize the disorder at the cellular level. ... the investigators also report their identification of a promising drug to reverse the heart malfunction - for which there are currently no decent treatments - after using these newly created heart cells to check the effects of a plethora of compounds.

College of Veterinary Medicine to perform an animal stem cell first

The first animal stem cell procedure in Oregon done entirely in a veterinary facility is scheduled for Thursday at the Oregon State University College of Veterinary Medicine. The procedure will be performed on Basco (pronounced "Bosco"), a 7-year-old German Shepherd suffering from osteoarthritis in his left rear hip. ... Fat tissue is removed from the animal, the stem cells are separated and activated, and then injected into the affected area. Within three to four weeks of the procedure, Basco should be moving well, with little or no pain, Medi-Vet predicted.

Veterinary medicine is far ahead in its application of first generation stem cell therapies; if you're a human in need of the same sort of treatment, you'll have to leave the US to find it. The principle effect of heavy US regulations on medical development is to ensure that working, beneficial, reasonably safe treatments take a very long time to come to the clinic and are very expensive when they arrive. Fortunately the FDA can't do anything about the competitive service providers and medical research and development groups in other parts of the world. Thus, absent a sea change in the state of regulation in the US, medical tourism will be a part of all our futures, and we will benefit greatly from the fact that at least some parts of the world are not as shackled and held back by a full-on command economy medical system.

I'm always pleased to see more good writing on the topic of longevity science: "To extend our longevity, we'll have to advance in stages. ... With a healthy lifestyle and some luck (absence of accidents and natural disasters) we not only can increase our lifespan, we can increase the health in that lifespan and postpone debilitating illness to the very end of our life ... To go beyond this achievable life extension, we need more advances in the basic sciences. Considering aging as a disease is new concept. It will take time before we accept this not just as wishful thinking but as a real possibility in our lifetime. The end of aging does not mean that we will never die; we will still die of other diseases, accidents, or natural disasters but no longer of aging itself. ... Aging is not yet recognized as a disease. Some among us would like the Food and Drug Administration (FDA) to recognize it as a disease so that we could get funding for basic, translational, and clinical research on aging. ... These changes will be implemented incrementally. The unprecedented biological and technological evolution we face today will be the driving force for social, economic, and even political changes. Working conditions will change significantly: retirement will be changed, people will no longer retire after a certain age, they will take time off from work every few years and then return to it afterwards. Our goal is not to reach immortality but to postpone and eventually prevent aging. For now and the immediate future we can change our lifestyle toward healthier living. This will buy us time so that we can survive long enough for the advances in basic sciences, which will be made in the next 15 to 20 years, helping us move to the next stage where aging will no longer be the biggest killer of our species."

Link: http://www.brooklyneagle.com/categories/category.php?id=41234

There is no shortage of people trying to convince us that degenerating into frailty, suffering, and death is a wonderful thing: "Mr Agronin is an optimist. He does not deny - how could he? - the sufferings and indignities of old age. Scanning slices of old brain, 'stained and prepped for the microscope', his eye is unsparing: 'the aged folds' like 'the withered meat of a walnut', the blood vessels like 'hardened tendrils', the 'small plaques of toxic amyloid protein surrounded by a debris field of dead neurons'. But alongside the science, he sees something else: the people themselves. Old age, he says, has become our blind spot, neglected by the medical profession, lumped together with dementia and disease, something to be endured, dreaded, mercifully pre-empted, or even - as one researcher in the field, Aubrey de Grey, argues - reversed. Mr Agronin, by contrast, embraces it. He sees it as intrinsic to life, with its own 'ways and meanings', its particular wisdom. Even at its most tenuous and hollowed out, he finds some shape, a sense of cyclic pattern. In an almost mystical passage, inspired by his professor, Erik Erikson, a psychologist, Mr Agronin likens life to a stream which eventually seeps down unseen into the bedrock, and opens 'like a flower into the aquifer below'." From where I stand, there needs to be more of a healthy dread of aging - perhaps that would motivate more people to help develop the rejuvenation biotechnologies that can do something about it. To try to pretend that aging to death, suffering terribly along the way, is just peachy keen has an air of desperate madness to it.

Link: http://www.economist.com/node/18111554

This research has been doing the rounds:

This week researchers from the Dana-Farber Cancer Institute reported that the length of telomeres - which shorten with age - determines virtually every aspect of aging from wrinkles and gray hair to the onset of dementia, diabetes, and heart disease. At least that was the case in the mice they studied in a report published in Nature.

"We think we've identified the core pathway that really helps explain many different theories of aging," says study co-author Dr. Ronald DePinho, a geneticist at Dana-Farber. "Our study provides a unified field theory for aging."

In a nutshell, once telomeres shorten to a particular length, aging accelerates. Shortened telomeres allow the cell's DNA to become damaged, which activates a gene, p53. This sets off a warning to shut down the cells' normal growth and division cycle until the damage can be fixed or, if not, the cells die. At the same time, cells with short telomeres have power plants, or mitochondria, that are no longer operating at full capacity. This leads to malfunction in crucial organs like the brain, heart, liver, and pancreas, as well as a loss of muscle, and eventually extreme weakness and frailty.

(The paper is at Nature if you're the sort who likes to read primary sources). That's an ambitious declaration from the researcher quoted above - I can only imagine it's taken somewhat out of context and then hyped up by the science writer for the introductory paragraph, as it is certainly the case that damaged mitochondria and shortening telomeres are only two of the possible reasons we suffer age-related degeneration. Many of the other causes of aging involve a build up of varying forms of damaging waste product that the body cannot remove - mechanisms which are quite capable of causing disability and death on their own, telomere shortening or no telomere shortening.

That said, telomeres, mitochondria, and p53 are all large and healthy areas of research when it comes to the biology of aging. I imagine that anyone would be pleased to produce good evidence that might mechanically tie them all together, such that one or more are secondary effects rather than primary causes. From an economic perspective, we should all be hoping that some of our present candidates for the primary causes of aging turn out to be secondary effects - because then we don't have to devote any time towards developing repair biotechnologies to fix them.

On a closer reading of the new research, I have to say that it looks to me very much like an independent confirmation of discoveries from 2007 and 2008 relating to mitochondrial damage, telomere length, and the enzyme telomerase. In a nutshell, it may be that telomere shortening is entirely driven by mitochondrial dysfunction:

Researchers have put forward evidence to suggest that telomere shortening is caused by accumulated damage to mitochondrial DNA - essentially collapsing two areas of intense interest for gerontologists down to one root cause, if confirmed. ... [It may be the case that] poorly functioning mitochondria lead to telomere shortening, and telomerase somehow improves mitochondrial function to prevent that shortening. This is in place of the more expected path of undoing ongoing telomere shortening by adding extra repeat sequences to the end of the telomeres - that being the better understood function of telomerase.

I don't immediately see anything in the Nature paper that would rule out this interpretation of the link between these two fundamental mechanisms of aging. Like the earlier researchers, this present group also found that boosting telomerase activity improved mitochondrial function, though I believe they are arguing that the improved function happens as a secondary result of interactions between telomere length and p53. There's certainly plenty of room amidst the uncertainty for contradictory interpretations at this stage.