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.
The rate at which cancer death rates decline from year to year has has improved.
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
Everything gives you cancer
Everything
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.