In testosterone-deficient men, major weight loss was an added benefit of testosterone replacement therapy for most of the patients who participated in a new study. The results will be presented Saturday at The Endocrine Society's 94th Annual Meeting in Houston.
"The substantial weight loss found in our study—an average of 36 pounds—was a surprise," said the study's lead author, Farid Saad, PhD, of Berlin-headquartered Bayer Pharma.
Although prior studies using testosterone therapy in testosterone-deficient men consistently show changes in body composition, such as increased lean mass and decreased fat mass, Saad said the net effect on weight seemed unchanged in those studies. However, Saad said their study, which took place in Germany, had a longer follow-up by at least two years and used long-acting injections of testosterone.
Also, testosterone decline is very often due to obesity and depression. So then weight gain and testosterone decline seem like a vicious cycle.
A new study finds that a drop in testosterone levels over time is more likely to result from a man's behavioral and health changes than by aging. The study results will be presented Monday at The Endocrine Society's 94th Annual Meeting in Houston.
"Declining testosterone levels are not an inevitable part of the aging process, as many people think," said study co-author Gary Wittert, MD, professor of medicine at the University of Adelaide in Adelaide, Australia. "Testosterone changes are largely explained by smoking behavior and changes in health status, particularly obesity and depression."
More sex will boost male testosterone levels. Sated lust is good for health.
A clinical trial of testosterone treatment in older men, reported June 30 online in the New England Journal of Medicine, has found a higher rate of adverse cardiovascular events, such as heart attacks and elevated blood pressure, in a group of older men receiving testosterone gel compared to those receiving placebo. Due to these events, the treatment phase of the trial was stopped. The study was supported by a grant to Shalender Bhasin, M.D., at Boston Medical Center from the National Institute on Aging (NIA), part of the National Institutes of Health.
Is it possible to use hormone supplementation to achieve a net health benefit? The answer is not clear. These men had an average age of 74 and existing health problems. Does testosterone cause problems with slightly younger and healthier men?
Decreased muscle strength may contribute to difficulties in mobility, such as in walking or climbing stairs, which can limit older persons’ independence. Testosterone treatment has been shown to improve muscle strength in some older men, but it is not yet known whether it would reduce mobility limitations in older men with low testosterone levels. The TOM (Testosterone in Older Men) Trial was designed to address this question. It was a randomized, double-blind, placebo-controlled clinical trial of the effects of six months of testosterone gel treatment on strength and ability to walk and climb stairs in 209 older men with low testosterone levels and mobility limitations. The testosterone gel used in this study was administered to the skin daily. The 209 men in the trial had an average age of 74 and high rates of chronic diseases such as diabetes and cardiovascular disease.
It is possible that at a younger age testosterone could deliver a net benefit. But this is speculation on my part. The problem is that as we age lots of mechanisms have gone so awry that stimulating them just causes them to go wrong faster. Though another recent study found that ovary transplants improve the health of aged female mice. Those ovaries pump out a lot of hormones and yet they deliver a net benefit. Maybe the reason the transplants deliver a net benefit is that the ovaries excrete multiple kinds of hormones and with hormone release patterns optimized to improve health. Internal organs have complex regulatory mechanisms. Whereas testosterone gels are not released in ways that precisely mimic what the brain will do.
Rome, Italy: Scientists have discovered that when they transplant ovaries from young mice into aging female mice, not only does the procedure make the mice fertile again, but also it rejuvenates their behaviour and increases their lifespan. The question now is: could ovarian transplants in women have the same effect?
Dr Noriko Kagawa will tell the 26th annual meeting of the European Society of Human Reproduction and Embryology in Rome today (Tuesday) that successful ovarian transplants increased the lifespan of the mice by more than 40%. "At present ovarian transplants are performed with the aim of preserving a woman's fertility after cancer treatment for instance, or of extending her reproductive lifespan. However, the completely unexpected extra benefit of fertility-preserving procedures in our mouse studies indicates that there is a possibility that carrying out similar procedures in women could lengthen their lifespans in general," she said.
Imagine transplanted ovaries that didn't pop out eggs but which did pump out hormones. A way to slow aging?
40% longer life thru ovary transplants.
Dr Kagawa said: "All the mice in both experiments that had received transplants resumed the normal reproductive behaviour of young mice. They showed interest in male mice, mated and some had pups. Normally, old mice stay in the corner of the cage and don't move much, but the activity of mice that had had ovarian transplants was transformed into that of younger mice and they resumed quick movements. Furthermore, the lifespan of the mice who received young ovaries was much longer than that of the control mice: the mice that had received two ovaries lived for an average of 915 days, and the mice that had received one ovary, for an average of 877 days. The newest of our data show the life span of mice that received transplants of young ovaries was increased by more than 40%.
With humans the ovary transplants might help. But resulting hormone surge might boost the risk of breast and cervical cancer. The net effect on human lifespans is hard to estimate at this point. Though the eventual development of cures for cancer would eliminate some of the downsides of ovary transplants and of other means to restore youthful hormone levels.
A protein called neuregulin 1 (NRG1) serves as a growth factor which when injected into mice causes muscle cells to replicate and repair damaged hearts.
Injured heart tissue normally can't regrow, but researchers at Children's Hospital Boston have now laid the groundwork for regenerating heart tissue after a heart attack, in patients with heart failure, or in children with congenital heart defects. In the July 24 issue of Cell, they show that a growth factor called neuregulin1 (NRG1), which is involved in the initial development of the heart and nervous system, can spur heart-muscle growth and recovery of cardiac function when injected systemically into animals after a heart attack.
I'm picturing people with heart disease buying this compound on the black market. Suppose it gets sold legally in any countries?
No need for embryonic stem cells or even adult stem cells. Muscle cells can be induced to start dividing.
After birth, heart-muscle cells (cardiomyocytes) normally withdraw from the cell cycle – meaning they stop dividing and proliferating. But the researchers, led by Bernhard Kühn, MD, and Kevin Bersell of the Department of Cardiology at Children's, were able to restart the cell cycle with NRG1, stimulating cardiomyocytes to divide and make copies of themselves -- even though they are not stem cells.
This makes me wonder what other adult fully differentiated post-mitotic (no longer dividing) cells in the body can be induced to start dividing again.
Ways of doing heart repair might be closer than we thought.
"Although many efforts have focused on stem-cell based strategies, our work suggests that stem cells aren't required and that stimulating differentiated cardiomyocytes to proliferate may be a viable alternative," says Kühn, the study's senior investigator and a practicing pediatric cardiologist at Children's since 2007.
Injection of neuregulin 1 (NRG1) and stimulation of production of a receptor for NRG1 caused heart muscle cell growth and improved heart function in mice.
When the team injected NRG1 into the peritoneal cavity of live mice after a heart attack, once daily for 12 weeks, heart regeneration was increased and pumping function (ejection fraction, assessed on echocardiograms) improved as compared with untreated controls. The NRG1-injected mice also lacked the left-ventricular dilation and cardiac hypertrophy that typify heart failure; both were seen in the controls.
When the researchers also stimulated production of a cellular receptor for NRG1, known as ErbB4, cardiomyocyte proliferation was further enhanced, demonstrating that NRG1 works by stimulating this receptor. They also identified the specific kinds of cardiomyocytes (mononucleated) that are most likely to respond to treatment.
Knowing how to repair our bodies as we age in very large part amounts to knowing how to instruct cells to fix everything that gets broken.
Update: Reason at the Fight Aging blog reports on another recent success in heart repair where Mayo Clinic researchers used induced pluripotent stem (iPS) cells to repair damaged hearts in mice. Because the heart is such a mechanical large sized device it seems a lot more amenable to repair than the brain or the spinal cord. I expect we'll stop suffering from heart disease before we stop suffering from strokes or dementia.
Knee surgery for osteoarthritis is big business but worthless. The lesson here is that we need stem cell therapies and other rejuvenating therapies. We need to reverse the processes of aging.
Running from 1999 to 2007, the study treated 178 London-area men and women with an average age of 60. All study participants received physical therapy as well as medications such as ibuprofen or acetaminophen, but 86 of the patients also received surgery consisting of lavage and arthroscopic debridement at LHSC. At several time intervals post-treatment, the researchers found both patient groups experienced comparable improvements in joint pain, stiffness, and function, but surgery provided no additional benefit.
Orthopedic surgeon and study co-author Dr. Bob Litchfield emphasizes this study addresses only arthritis-related knee problems. "Although this study did not show a significant therapeutic benefit of arthroscopic debridement in this patient population, knee arthroscopy is still beneficial in many other conditions affecting the knee, such as meniscal repair and resection, and ligament reconstruction." Litchfield is the Medical Director of the Fowler Kennedy Sport Medicine Clinic. He's also a professor In the Department of Surgery at Western's Schulich School of Medicine & Dentistry and a scientist with the Lawson Health Research Institute. "As surgeons, we need to know when things are working and when they're not. If this particular technique is not working for this subgroup of patients, we better come up with something else that does."
A 2002 study demonstrating similar results to this study was broadly dismissed by the medical community, and arthroscopic surgery of the knee remains a common treatment for joint pain and stiffness. But in this latest study the researchers conclude "based on the available evidence, we believe that the resources currently allocated towards arthroscopic surgery for osteoarthritis would be better directed elsewhere."
If you have parts that are worn out the solution is to make those parts young again. Surgery by itself can't do that. So surgery does not help.
(BRONX, NY) — As people age, their cells become less efficient at getting rid of damaged protein — resulting in a buildup of toxic material that is especially pronounced in Alzheimer's, Parkinson's disease, and other neurodegenerative disorders.
Now, for the first time, scientists at the Albert Einstein College of Medicine of Yeshiva University have prevented this age-related decline in an entire organ — the liver — and shown that, as a result, the livers of older animals functioned as well as they did when the animals were much younger. Published in the online edition of Nature Medicine, these findings suggest that therapies for boosting protein clearance might help stave off some of the declines in function that accompany old age. The study's senior author was Dr. Ana Maria Cuervo, associate professor in the departments of developmental & molecular biology, medicine and anatomy & structural biology at Einstein.
A declining ability to take out intracellular trash is one of the causes of aging. Though apparently some scientists are not convinced yet.
The cells of all organisms have several surveillance systems designed to find, digest and recycle damaged proteins. Many studies have documented that these processes become less efficient with age, allowing protein to gradually accumulate inside cells. But aging researchers continue debating whether this protein buildup actually contributes to the functional losses of aging or instead is merely associated with those losses. The Einstein study was aimed at resolving the controversy.
The chaperone system of intracellular removal of damaged proteins declines with age and Dr. Cuervo targeted it for genetic enhancement to keep it going stronger as mice age.
One of these surveillance systems — responsible for handling 30 percent or more of damaged cellular protein — uses molecules known as chaperones to seek out damaged proteins. After finding such a protein, the chaperone ferries it towards one of the cell's many lysosomes — membrane-bound sacs filled with enzymes. When the chaperone and its cargo "dock" on a receptor molecule on the lysosome's surface, the damaged protein is drawn into the lysosome and rapidly digested by its enzymes.
In previous work, Dr. Cuervo found that the chaperone surveillance system, in particular, becomes less efficient as cells become older, resulting in a buildup of undigested proteins within the cells. She also detected the primary cause for this age-related decline: a fall-off in the number of lysosomal receptors capable of binding chaperones and their damaged proteins. Could replenishing lost receptors in older animals maintain the efficiency of this protein-removal system throughout an animal's lifespan and, perhaps, maintain the function of the animal's cells and organs as well?
To find out, Dr. Cuervo created a transgenic mouse model equipped with an extra gene — one that codes for the receptor that normally declines in number with increasing age. Another genetic manipulation allowed Dr. Cuervo to turn on this extra gene only in the liver and at a time of her choosing, merely by changing the animals' diet.
To keep the level of the receptor constant throughout life, Dr. Cuervo waited until mice were six months old (the age that the chaperone system's efficiency begins to decline) before turning on the added receptor gene. When the mice were examined at 22 to 26 months of age (equivalent to approximately 80 years old in humans), the liver cells of transgenic mice digested and recycled protein far more efficiently than in their normal counterparts of the same age — and, in fact, just as efficiently as in normal six-month old mice.
But will this bit of genetic engineering extend the lives of mice? Consider that if all it took to make livers last longer was to add a copy of a gene that evolution probably would have caused that change to happen already. Mutations that just create an extra copy of a gene have happened many times and we have lots of genes in us with multiple extra copies. So if this really helps why don't mice already have this mutation?
In older men with low testosterone levels, testosterone replacement therapy improves their risk factors for cardiovascular disease and diabetes, according to two new studies. The results will be presented at The Endocrine Society's 90th Annual Meeting in San Francisco.
Testosterone deficiency becomes more common with age, occurring in 18 percent of 70-year-olds, said a coauthor of both studies, Farid Saad, PhD, of Berlin-headquartered Bayer Schering Pharma. Low testosterone levels are linked to the metabolic syndrome—a cluster of metabolic risk factors that increase the chances of developing heart disease, stroke, and type 2 diabetes—and other health problems, including loss of bone and muscle mass, depression, and decreased libido.
Yet the risks and benefits of hormone replacement therapy are unclear in older men, he said.
Saad's research showed that restoring testosterone to normal levels in hypogonadal, or testosterone-deficient, men led to major and progressive improvements in features of the metabolic syndrome. Furthermore, men older than 63 benefited as much as younger men, they found. Treatment lasted a year and used a slow-release, injectable form of the hormone (testosterone undecanoate) that is not yet available in the United States.
All the men in this study have the metabolic syndrome that is correlated with high risk of heart disease and other diseases related to problems with the cardiovascular system. So if you do not have the metabolic syndrome these results do not mean that testosterone replacement will help you. It might not help you even if you do have metabolic syndrome.
All 95 men in the studies (ages 34 to 69 years) had the metabolic syndrome. To receive this diagnosis, patients must have three of the following five risk factors: increased waist circumference (abdominal fat), low HDL ("good") cholesterol, high triglycerides (fats in the blood), high blood pressure, and high blood sugar.
The testosterone improved an assortment of markers.
The first study showed that testosterone treatment significantly reduced waist circumference, total cholesterol, LDL ("bad") cholesterol, triglycerides, and body mass index (a measure of body fat). Treatment also increased "good" cholesterol. Improvements were progressive over 12 months, indicating that benefits may continue past a year, Saad said.
In the second study, the researchers divided the patient population into three groups by age: less than 57 years, 57 to 63 years, and more than 63 years. They found that the oldest men had similar improvements in metabolic risk factors to the youngest men.
Additionally, the investigators looked at the degree of testosterone deficiency before treatment. This beginning level of testosterone deficiency did not predict the beneficial outcome, they found. Men whose subnormal testosterone levels were not as low as the others had similar improvements in metabolic risk factors to men with the lowest levels, according to Saad.
"We conclude that if elderly men have a deficiency of testosterone, it is worthwhile to treat them with testosterone," he said.
What I wonder: If testosterone replacement is so beneficial why is it necessary in the first place?
My worry is that testosterone might drop in order to reduce the risk of prostate cancer and perhaps other cancers and diseases. One of the reasons various aspects of metabolism get turned down as we get older is probably an evolutionarily selected for risk reduction against cancer. Cells that divide less often are less prone to becoming cancerous because each cell division runs the risk of a mutation that makes the cell divide out of control.
But it is possible that medical researchers will be able to identify subsets of the population which could see a net decrease in mortality risk from a hormone replacement therapy. A more precise and custom tuning of metabolic function based on a scientific method of assessing the sizes of various risks for each person might turn up people who can benefit from testosterone replacement or some other hormone replacement. Not saying this is possible now. But it might become possible later.
A German study finds that men with lower testosterone have a greater risk of dying. But note this study does not demonstrate the direction of cause and effect. Maybe illness and faster aging lower the testosterone levels and that faster aging might precede the lowering of testosterone.
Men may not live as long if they have low testosterone, regardless of their age, according to a new study. The results will be presented at The Endocrine Society's 90th Annual Meeting in San Francisco.
The new study, from Germany, adds to the scientific evidence linking deficiency of this sex hormone with increased death from all causes over time—so-called "all-cause mortality."
The results should serve as a warning for men with low testosterone to have a healthier lifestyle, including weight control, regular exercise and a healthy diet, said lead author Robin Haring, a PhD student from Ernst-Moritz-Arndt University of Greifswald, Institute for Community Medicine.
"It is very possible that lifestyle determines levels of testosterone," he said.
In the study, Haring and co-workers looked at death from any cause in nearly 2,000 men aged 20 to 79 years who were living in northeast Germany and who participated in the Study of Health in Pomerania (SHIP). Follow-up averaged 7 years. At the beginning of the study, 5 percent of these men had low blood testosterone levels, defined as the lower end of the normal range for young adult men. The men with low testosterone were older, more obese, and had a greater prevalence of diabetes and high blood pressure, compared with men who had higher testosterone levels, Haring said.
Men with low testosterone levels had more than 2.5 times greater risk of dying during the next 10 years compared to men with higher testosterone, the study found. This difference was not explained by age, smoking, alcohol intake, level of physical activity, or increased waist circumference (a risk factor for diabetes and heart disease), Haring said.
In cause-specific death analyses, low testosterone predicted increased risk of death due to cardiovascular disease and cancer but not death of any other single cause.
The fact that low testosterone levels are linked not only to cardiovascular but also to cancer is very interesting. Does testosterone strengthen the immune system to beat down cancer at an early stage? What would explain this result?
Pro baseball players might get a performance boost from testosterone supplements. But a study of some old guys in the Netherlands found testosterone supplements for low testosterone old guys didn't boost their performance.
Older men with low testosterone levels who received testosterone supplementation increased lean body mass and decreased body fat, but were no stronger and had no improvement in mobility or cognition compared with men who did not use the supplement, according to a study in the January 2 issue of JAMA.
I find it surprising the men had more lean muscle mass but weren't any stronger. However, a lot of guys would enjoy the decrease in body fat since they'd look better.
“Male aging is associated with a gradual but progressive decline in serum levels of testosterone, occurring to a greater extent in some men than in others. Decline in testosterone is associated with many symptoms and signs of aging such as a decrease in muscle mass and muscle strength, cognitive decline, a decrease in bone mass, and an increase in (abdominal) fat mass,” the authors write. Clinical trials examining whether testosterone supplementation provides benefits or adverse effects have yielded mixed findings.
Marielle H. Emmelot-Vonk, M.D., of University Medical Center Utrecht, the Netherlands, and colleagues conducted a randomized, placebo-controlled study to assess the effects of testosterone supplementation on functional mobility, cognition, bone mineral density, body composition, lipids, quality of life, and safety parameters in older men with testosterone levels less than 13.7 nmol/L (less than the average level in this age group) during a period of six months. The trial, conducted from January 2004 to April 2005, included 207 men between the ages of 60 and 80 years. Participants were randomly assigned to receive 80 mg of testosterone undecenoate or a matching placebo twice daily for six months.
The results were mixed. I think what is needed is a much longer term study so that differences in all cause mortality could become clear.
The researchers found that during the study, lean body mass increased and fat mass decreased in the testosterone group compared with the placebo group but these factors were not accompanied by an increase of functional mobility or muscle strength. Cognitive function and bone mineral density did not change. Insulin sensitivity improved but high-density lipoprotein cholesterol (the “good” cholesterol) decreased. By the end of the study, 47.8 percent in the testosterone group vs. 35.5 percent in the placebo group had the metabolic syndrome (a strong risk factor for cardiovascular disease and type 2 diabetes, a group of several metabolic components in one individual including obesity and dyslipidemia). This difference was not statistically significant.
Quality-of-life measures did not differ aside from hormone-related quality of life in the testosterone group. Adverse events were not significantly different in the two groups. Testosterone supplementation was associated with an increase in the concentrations of blood creatinine, a measure of kidney function, and hemoglobin and hematocrit, two red blood cell measures. No negative effects on prostate safety were detected (some reports have suggested that testosterone therapy could increase the risk of development or progression of prostate disease or cancer).
This is an important study because the differences in testosterone levels were caused by testosterone supplementation, not by naturally occurring differences between people. Other studies have found indications of possible benefit from having naturally occurring higher testosterone. See my posts Low Testosterone Men Die More Rapidly and Low Testosterone Men Die Sooner and Higher Testosterone Men Face Lower All Cause Mortality. But these studies on naturally occurring testosterone levels do not demonstrate the order of cause and effect. It could be that the men with higher testosterone have higher testosterone because they are more healthy. Maybe their genes cause them to age more slowly and age-adjusted relative youthfulness of their bodies allows their bodies to make more testosterone.
We need long term double blind controlled clinical studies of testosterone supplementation to find out if it is a net help or net harm. We simply do not know at this point. Personally, I'd rather have rejuvenated stem cell therapies, gene therapies, and nanomachine repair devices injected into me (at least as long as they won't take over my brain). I don't hold out big hopes for hormone supplementation therapies. We need to fix and replace what wears out. For that we need gene therapies and cell therapies.
A new report from the nation’s leading cancer organizations shows cancer death rates decreased on average 2.1 percent per year from 2002 through 2004, nearly twice the annual decrease of 1.1 percent per year from 1993 through 2002. The findings are in the “Annual Report to the Nation on the Status of Cancer, 1975-2004, Featuring Cancer in American Indians and Alaska Natives” published online October 15, 2007 (www.interscience.wiley.com/cancer/report2007) and appearing in the November 15, 2007, issue of Cancer.
A featured special section provides the most comprehensive cancer data to date for American Indians and Alaska Natives (AI/AN) across the United States. Cancer incidence rates among AI/AN men and women varied two-fold among six geographic regions of the country. From 1999 through 2004, AI/AN men from the Northern Plains region and AI/AN women from Alaska and the Northern and Southern Plains regions had higher cancer incidence rates than non-Hispanic white (NHW) men and women in the same areas.
Among the general population, the report shows that long-term declines in cancer death rates continued through 2004 for both sexes and, despite overall higher death rates for men, the declines from 2002 through 2004 were 2.6 percent per year among men and 1.8 percent per year among women. Death rates decreased for the majority of the top 15 cancers in men and women. Important declines were noted for the three leading causes of cancer deaths in men: lung, prostate and colorectal cancers. In women, deaths rates from colorectal cancer and breast cancer decreased, while the rate of increase for lung cancer deaths slowed substantially.
Progress does not run at a constant rate. At some point curing cancer is going to become easy. Looking at big mainframe computer boxes in the 1970s most would not have guessed what was coming. We now can do things with computers that give us enormous power. Microfluidic devices, built using technologies developed in the computer industry, are going to greatly accelerate the rate of advance in medical science and biotechnology. We will gain the ability to manipulate cells and components of cells with the precision needed to figure out and cure cancer. Just as the computer industry has gained the ability to manipulate smaller and smaller pieces of matter so will the biomedical industry.
Calorie restriction extends life in most animals which have been studied well on calorie restricted diets. Calorie restriction is the only consistent way to extend life in lab animals that has been found to date. Some University of Florida scientists found that rats on low calorie diets might live longer because the calorie restriction causes cells to more rapidly chew up and recycle cellular components such as energy-producing mitochondria.
And a University of Florida study shows just how much the body benefits when it “goes green,” at least if you’re a rat: Cutting calories helps rodents live longer by boosting cells’ ability to recycle damaged parts so they can maintain efficient energy production.
“Caloric restriction is a way to extend life in animals. If you give them less food, the stress of this healthy habit actually makes them live longer,” said Christiaan Leeuwenburgh, Ph.D., chief of the division of biology of aging in UF’s Institute on Aging.
Understanding how the process works at the cellular level in rodents could help scientists develop drugs that mimic the process in humans, Leeuwenburgh added.
Some biogerontologists theorize that aging damaged mitochondria displace healthy mitochondria. Then those damaged mitochondria spew out free radicals that damage cells. These University of Florida researchers are speculating that if cells more aggressively chew up damaged mitochondria then those bad mitochondria won't take over and squeeze out healthier mitochondria.
Fortunately, younger cells are adept at reducing, recycling and rebuilding.
In this process, damaged mitochondria are quickly swallowed up and degraded. The broken down pieces are then recycled and used to build new mitochondria. However, older cells are less adept at this process, so damaged mitochondria tend to accumulate and contribute to aging.
Here is their core finding. Calorie restriction accelerated autophagy, the recycling of damaged cellular components.
UF scientists studied 22 young and old rats, comparing those allowed to eat freely with those fed a low-calorie, nutritious diet.
The stress of a low-calorie diet was enough to boost cellular cleaning in the hearts of older rats by 120 percent over levels seen in rats that were allowed to eat what they wanted. The diet had little or no effect on younger rats.
If drugs could be found that enhance autophagy (the chewing up of damaged cellular components) then those drugs might slow down the aging process by preventing bad damaged mitochondria from taking over cells and spewing free radicals into cells and into the environment around cells.
“Autophagy is a housekeeping mechanism that keeps cells free of damaged and thereby detrimental mitochondria and other toxic materials while recycling their building blocks — nutrients needed by the cell,” said Stephanie Wohlgemuth, Ph.D., a lecturer in UF’s department of aging and geriatrics and the study’s lead author. “So if that process is maintained with age – or even increased – that can only be beneficial.”
Gene therapy that could fix mitochondrial DNA might some day deliver an even bigger anti-aging benefit by fixing damaged mitochondria that spew free radicals.
An organization called Partnership for Prevention claims 5 preventive measures could save over 100,000 lives per year
I'm skeptical of the wisdom behind the first claim about aspirin use. The evidence on aspirin use for low risk patients is ambiguous. Though prolonged aspirin use might lower the risk of cancer. Also, I'm surprised to see the claim about flu vaccines. Influenza vaccination might not reduce mortality in the elderly. (more here) Though if everyone got vaccinated then the elderly would face less risk of getting exposed to an infected person. The best vaccination strategy depends on the transmissibility of each strain.
Screening for cancer is probably a net benefit. Cancers caught and removed sooner are cancers less likely to have metastatized before removal. So their cancer recommendations (at least for colonoscopy) are probably at least approximately correct. What would really benefit us: implantable cancer detector devices. Detect cancer every day with embedded sensors that could use radio waves to report to an external computer whether a cancer has been detected.
For your heart my advice is to improve your diet and get more exercise. Exercise and better diet are more assured methods of reducing heart disease risk. Eat like an ape man.
I hear Joe Jackson singing:
Everything gives you cancer
Everything gives you cancer
Theres no cure, theres no answer
Everything gives you cancer
You want benefits without costs? Keep looking. Cholesterol-lowering statin drugs probably cause a small boost in the risk of cancer.
Millions of Americans take statins to lower their cholesterol, but how low should you go" Many scientific studies support the benefits of lowering low-density lipoprotein (LDL) cholesterol, and achieving low LDL cholesterol levels is one of the most important steps in preventing heart disease. New research, however, provides evidence for an association between low LDL levels and cancer risk.
The authors of the study, published in the July 31, 2007, issue of the Journal of the American College of Cardiology (JACC), set out to understand how and why statins cause side effects, particularly damage to the liver and muscle cells. The study findings support taking multiple medications rather than high-dose statins to minimize those side effects. The researchers did not expect to find the increased cancer risk (one additional incident per 1,000 patients) from low LDL levels, and additional studies have already begun to investigate this potential risk further. A key component in future studies will be to confirm the risk and to identify whether the risk may be a side effect of statins or just low LDL.
“This analysis doesn’t implicate the statin in increasing the risk of cancer,” said lead author Richard H. Karas, M.D., F.A.C.C., professor of medicine at Tufts University School of Medicine. “The demonstrated benefits of statins in lowering the risk of heart disease remain clear; however, certain aspects of lowering LDL with statins remain controversial and merit further research.”
The researchers found one additional incident of cancer per 1,000 patients with low LDL levels when compared to patients with higher LDL levels. In their evaluation of randomized controlled statin trials published before November 2005, the researchers looked at 13 treatment arms consisting of 41,173 patients.
Do the statins directly cause damage to cells that leads to cancer? Or does the lowering of cholesterol somehow remove some brakes on cancer cell growth?
Keep in mind that statins lower risk of death from heart disease more than they increase the risk from cancer. Plus, the statin simvastatin appears to lower the risk of Parkinson's and Alzheimer's diseases.
If you want to lower your cholesterol without taking statins then try the ape diet.
Get on the cutting edge. States where people take the latest drugs have longer life expectancies.
It is no surprise that Americans are living longer today than in previous generations. A typical baby born in 1900 was expected to live to about age 45. Today, life expectancy at birth is about 78. Less well known, however, is the fact that the gains in life expectancy have not been uniform across the country. In his new study—the first of its kind—Columbia University researcher Frank Lichtenberg set out to find out which states are the leaders, which ones are the laggards, and why.
Lichtenberg began by constructing life-expectancy estimates of residents in all fifty states using data from the National Center for Health Statistics. He found that in 2004, on average, residents of Hawaii (81.3 years) and Minnesota (80.3 years) lived six or seven years longer than residents of Mississippi and Louisiana (74.2 years).
In addition, he found that while nationwide life expectancy increased by 2.33 years from 1991 to 2004, the increase varied greatly among the states. Certain states—New York (4.3 years), California (3.4 years), and New Jersey (3.3 years)—led the way, while others–Oklahoma (0.3 years), Tennessee (0.8 years), and Utah (0.9 years) trailed the national average by significant margins.
See the full article for a list of life expectancies by state. But since there are differences in life expectancy due to genetic effects of race and ethnicity and also due to regional dietary differences and other causes you can't assume that moving to a state with higher average life expectancy will increase your own life expectancy. Better to adopt life extending practices right where you are.
The newer the average age of used drugs the greater the increase in longevity. This argues against use of generic drugs (though they can be best of breed in some cases).
Lichtenberg then set out to examine why this “longevity increase gap” exists by measuring the impact of several factors that researchers agree could affect life expectancy. He found that, although some obvious suspects—obesity, smoking, and the incidence of HIV/AIDS—played a role, the most important factor was “medical innovation.”Specifically, Lichtenberg found that longevity increased the most in those states where access to newer drugs—measured by mean “vintage” (FDA approval year)—in Medicaid and Medicare programs has increased the most. In fact, about two-thirds of the potential increase in longevity—the longevity increase that would have occurred if obesity, income, and other factors had not changed—is attributable to the use of newer drugs. According to his calculations, for every year increase in drug vintage there is about a two-month gain in life expectancy. These represent important findings given the fact that the costs of prescription drugs continue to receive a great deal of attention in the ongoing debate over health-care policy, while their benefits are often overlooked.
Attempts to regulate and reduce drug prices will slow the growth rate in longevity by reducing the economic incentive to develop new drugs. We need more new drug development. More new chemical compound drugs can raise life expectancy even further. But we need to move to new types of medical treatments in order to achieve a really big burst in medical treatment efficacy. In particular, stem cells, gene therapies, and nanodevices will some day stop aging altogether and even reverse the aging process.
Economists who favor ever increasing income growth need to come up with an answer to Lichtenberg's claim that rising incomes work against growth in life expectancy.
• Growth in obesity and, interestingly, growth in income were both inversely related to (and presumably reduced) the growth in life expectancy.
• If obesity and income had not increased, life expectancy at birth would have increased by 3.88 years from 1991 to 2004, instead of the actual 2.33-year increase. Thus, 3.88 years is the “potential increase in life expectancy at birth.”
• Of the 3.88-year potential increase in life expectancy at birth, medical innovation (i.e., the increase in Medicaid and Medicare drug vintage) accounted for 2.43 years (63%). The declines in AIDS incidence and smoking accounted for 0.23 and 0.12 years (6% and 3%), respectively. About 1.1 years (28%) of the potential increase in life expectancy at birth is unexplained.
• If obesity and income had not increased, life expectancy at age 65 would have increased by 2.15 years from 1991 to 2004, instead of the actual 1.29-year increase. Thus, 2.15 years is the “potential increase in life expectancy at age 65.”
• Of the 2.15-year potential increase in life expectancy at age 65, medical innovation (i.e., the increase in Medicaid and Medicare drug vintage) accounted for 1.19 years (55%). The declines in AIDS incidence and smoking accounted for 0.07 and 0.12 years (3% and 5%), respectively. About 0.8 years (36%) of the potential increase in life expectancy at age 65 is unexplained.
Did the income growth come as a result of harder worker and more daily stress? Or does the income effect come because people who do less physical work earn more money on average but get less daily exercise?
I see the effects of rising incomes as a mixed bag. On the positive side (and probably more important in the long run), people with higher incomes can afford to pay more for health care directly and through taxes. Their high incomes provide the incentives for medical centers and drug companies to develop new treatments. Rising affluence makes more money available for medical care and for research.
Rising affluence also allows more people to do science and technology because a declining portion of the population needs to grow food and do other basic activities needed for short term survival. The general advance in science and technology produces technologies from other industries which greatly speed up work in biomedical research laboratories.
When gene therapies, stem cell therapies, replacement organ growth techniques, and nano repair devices become usable in medical treatment we are going to witness an increase in life expectancy measured in decades and centuries. What we are seeing now with our latest drugs is a small harbinger of what will come.