Just in time for Valentine’s Day, a test to check your IQ of Sex & Love. Research shows a link between romantic love with sex. In recent years, researchers have focused their attention on the complex interplay between attachment processes and the sexual aspects of romantic love.

Reviewing research that explore men’s and women’s cognitions (knowledge and beliefs) about the nature of romantic love. The most commonly generated characteristics were trust, sexual attraction/desire and acceptance/tolerance. This support the hypothesis that the concept of romantic love is prototypically organized (i.e. has an internal structure), and that sexual desire is one of the central features of this concept.

Click this link to begin the The Valentine Quiz: Test Your Knowledge of Sex & Love findout your Sex & Love I.Q.


Protein helps parasite survive in host cells br  | Newsroom | Washington University in St. Louis.

Men Over 75 Still Sexually Active – Sexual Health (Healthy Sex, Sexual Relationships, Diseases, and Infections) on MedicineNet.com.

MIT researchers reported in Nature results that counter the idea that oxygen free radicals cause aging, instead that calorie restriction prolongs life because it increases respiration, not because it decreases oxygen free radicals.

MIT biologist Leonard Guarente believes “the conventional wisdom on oxygen radicals is dead wrong. Our results (in yeast) are contrary to the frequent suggestion that calorie restriction functions by slowing metabolism and thereby slowing the generation of free radicals.”

Guarente, who is working on a book on aging to be published this fall, discovered in 2000 that calorie restriction activates the silenced information regulator (SIR2) gene, which has the apparent ability to slow aging. This gene makes a protein called Sir2, which Guarente has shown is integrally tied to extending life span in yeast and in the roundworm. Humans carry a similar gene.

Rather than a slower metabolism leading to a slower rate of respiration, it turns out that respiration in yeast cells under calorie restriction goes up, not down. “The increase in anti-oxidant enzymes that is reported to occur during calorie restriction in animals may be a result of an increase in respiration rather than a cause of the observed longevity,” Guarente said.

“A high respiration rate is intimately connected with calorie restriction in yeast,” he said. “A high respiration rate activates SIR2. When respiration goes up, NAD (nicotinamide adenine dinucleotide, a co-enzyme that activates SIR2) goes up and SIR2 goes up. When SIR2 goes up, longevity happens.”


The prospect of a possible future drug seems too good to be true: Lose weight and live longer. Guarente’s aim is just such a drug.

Calorie restriction extends life span in a wide spectrum of organisms. It is the only regimen known to lengthen the life span of mammals such as mice and rats. One conventional theory for why this works is that to conserve energy and live within the means of limited food intake, the organism’s metabolism slows down.

Because a 30 percent reduction in calories is too difficult for most people to maintain, Guarente hopes to find the knowledge that would allow a pharmacological “trick” to make the organism think that it is calorie-restricted even when it is not. The hoped-for result is that this will trigger longevity.


When a yeast cell metabolizes food, the process can lead to respiration or fermentation, both of which supply the cell with energy.
When there is plenty of food available, yeast cells prefer to use food for fermentation. When food is scarce, the cell opts for respiration. Guarente found that this metabolic shift toward respiration increases SIR2’s activity and thus life span, just as calorie restriction does.

In mammals, excess carbon is used to make fatty acids and store carbohydrates. If there is a way to mimic this metabolic shift in humans, it would mean that more food would be used for respiration and less would be stored as fat. The result? We could live longer and be thinner.


Studies have suggested that calorie restriction slows aging primarily because it decreases oxygen free radicals. Oxygen free radicals are byproducts of oxidation, the body’s process of turning oxygen into energy.

Free radicals are thought to be toxic, causing damage to DNA and cells. Although antioxidants “clean up” free radicals, this process becomes more inefficient as we age. Many scientists speculate that free radical damage is the primary culprit behind age-related diseases and the symptoms of aging.

Contrary to these previous findings, Guarente says in the current paper that oxygen free radicals do not limit the reproductive life span of yeast and are not central to the extension of life span by calorie restriction.

Co-authors for the paper are Su-Ju Lin, Matt Kaeberlein, Pierre-Antoine Defossez of the MIT Department of Biology; biology graduate student Alex A. Andalis and MIT Professor of Biology Gerald Fink of the Whitehead Institute for Biomedical Research and Lori A. Sturtz and Valerie C. Culotta of the Johns Hopkins School of Public Health.
This work is supported by the National Institutes of Health, the Ellison Medical Foundation, the Seaver Institute and the Howard and Linda Stern Fund.


Article adapted by MD Only from original press release.


Contact: Deborah Halber
MIT News.

University of California, Berkeley, scientists, however, have found a welcome reason to delve into your genetic heritage: to find the slight genetic flaws that can be fixed with remedies as simple as vitamin or mineral supplements.

“I’m looking for the good news in the human genome,” said Jasper Rine, UC Berkeley professor of molecular and cell biology.

“Headlines for the last 20 years have really been about the triumph of biomedical research in finding disease genes, which is biologically interesting, genetically important and frightening to people who get this information,” Rine said. “I became obsessed with trying to decide if there is some other class of information that will make people want to look at their genome sequence.”

What Rine and colleagues found and report this week in the online early edition of the journal Proceedings of the National Academy of Sciences (PNAS) is that there are many genetic differences that make people’s enzymes less efficient than normal, and that simple supplementation with vitamins can often restore some of these deficient enzymes to full working order.

First author Nicholas Marini, a UC Berkeley research scientist, noted that physicians prescribe vitamins to “cure” many rare and potentially fatal metabolic defects caused by mutations in critical enzymes. But those affected by these metabolic diseases are people with two bad copies, or alleles, of an essential enzyme. Many others may be walking around with only one bad gene, or two copies of slightly defective genes, throwing their enzyme levels off slightly and causing subtle effects that also could be eliminated with vitamin supplements.

Electron microscope image of budding yeast
Electron microscope image of budding yeast,Saccharomyces cerevisiae. UC Berkeley researchers insert variants of human enzymes into yeast to see if these enzymes can be tuned up with vitamins. (UC Berkeley)

“Our studies have convinced us that there is a lot of variation in the population in these enzymes, and a lot of it affects function, and a lot of it is responsive to vitamins,” Marini said. “I wouldn’t be surprised if everybody is going to require a different optimal dose of vitamins based on their genetic makeup, based upon the kind of variance they are harboring in vitamin-dependent enzymes.”

Though this initial study tested the function of human gene variants by transplanting them into yeast cells, where the function of the variants can be accurately assessed, Rine and Marini are confident the results will hold up in humans. Their research, partially supported by the Defense Advanced Research Projects Agency (DARPA) and the U.S. Army, may enable them to employ U.S. soldiers to test the theory that vitamin supplementation can tune up defective enzymes.

“Our soldiers, like top athletes, operate under extreme conditions that may well be limited by their physiology,” Rine said. “We’re now working with the defense department to identify variants of enzymes that are remediable, and ultimately hope to identify troops that have these variants and test whether performance can be enhanced by appropriate supplementation.”

In the PNAS paper, Rine, Marini and their colleagues report on their initial analysis of variants of a human enzyme called methylenetetrahydrofolate reductase, or MTHFR. The enzyme, which requires the B vitamin folate to work properly, plays a key role in synthesizing molecules that go into the nucleotide building blocks of DNA. Some cancer drugs, such as methotrexate, target MTHFR to shut down DNA synthesis and prevent tumor growth.

Using DNA samples from 564 individuals of many races and ethnicities, colleagues at Applied Biosystems of Foster City, Calif., sequenced for each person the two alleles that code for the MTHFR enzyme. Consistent with earlier studies, they found three common variants of the enzyme, but also 11 uncommon variants, each of the latter accounting for less than one percent of the sample.

They then synthesized the gene for each variant of the enzyme, and Marini, Rine and their UC Berkeley colleagues inserted these genes into separate yeast cells in order to judge the activity of each variant. Yeast use many of the same enzymes and cofactor vitamins and minerals as humans and are an excellent model for human metabolism, Rine said.

The researchers found that four different mutations affected the functioning of the human enzyme in yeast. One of these mutations is well known: Nearly 30 percent of the population has one copy, and nine percent has two copies.

The researchers were able to supplement the diet of the cultured yeast with folate, however, and restore full functionality to the most common variant, and to all but one of the less common variants.

Structure of the active site of the methylenetetrahydrofolate reductase enzyme in bacteria
Structure of the active site of the methylenetetrahydrofolate reductase enzyme in bacteria (E. coli), which is similar to the structure of the yeast MTHFR enzyme. The five sites labeled in red are places where common mutations occur affecting the enzyme’s activity; mutations at the green-labeled site do not affect the enzyme’s activity. (Geoff Horner/UC Berkeley)

Since this experiment, the researchers have found 30 other variants of the MTHFR enzyme and tested about 15 of them, “and more than half interfere with the function of the enzyme, producing a hundred-fold range of enzyme activity. The majority of these can be either partially or completely restored to normal activity by adding more folate. And that is a surprise,” Rine said.

Most scientists think that harmful mutations are disfavored by evolution, but Rine pointed out that this applies only to mutations that affect reproductive fitness. Mutations that affect our health in later years are not efficiently removed by evolution and may remain in our genome forever.

The health effects of tuning up this enzyme in humans are unclear, he said, but folate is already known to protect against birth defects and seems to protect against heart disease and cancer. At least one defect in the MTHFR enzyme produces elevated levels in the blood of the metabolite homocysteine, which is linked to an increased risk of heart disease and stroke, conditions that typically affect people in their post-reproductive years.

“In those people, supplementation of folate in the diet can reduce levels of that metabolite and reduce disease risk,” Marini said.

Marini and Rine estimate that the average person has five rare mutant enzymes, and perhaps other not-so-rare variants, that could be improved with vitamin or mineral supplements.

“There are over 600 human enzymes that use vitamins or minerals as cofactors, and this study reports just what we found by studying one of them,” Rine said. “What this means is that, even if the odds of an individual having a defect in one gene is low, with 600 genes, we are all likely to have some mutations that limit one or more of our enzymes.”

The subtle effects of variation in enzyme activity may well account for conflicting results of some clinical trials, including the confusing data on the effect of vitamin supplements, he noted. In the future, the enzyme profile of research subjects will have to be taken into account in analyzing the outcome of clinical trials.

If one considers not just vitamin-dependent enzymes but all the 30,000 human proteins in the genome, “every individual would harbor approximately 250 deleterious substitutions considering only the low-frequency variants. These numbers suggest that the aggregate incidence of low-frequency variants could have a significant physiological impact,” the researchers wrote in their paper.

All the more reason to poke around in one’s genome, Rine said.

“If you don’t give people a reason to become interested in their genome and to become comfortable with their personal genomic information, then the benefits of much of the biomedical research, which is indexed to particular genetic states, won’t be embraced in a time frame that most people can benefit from,” Rine said. “So, my motivation is partly scientific, partly an education project and, in some ways, a partly political project.”

Marini and Rine credit Bruce Ames, a UC Berkeley professor emeritus of molecular and cell biology now on the research staff at Children’s Hospital Oakland Research Institute, with the research that motivated them to look at enzyme variation. Ames found in the 1970s that many bacteria that could not produce a specific amino acid could do so if given more vitamin B6, and in recent years he has continued exploring the link between micronutrients and health.

“Looked at in one way, Bruce found that you can cure a genetic disease in bacteria by treating it with vitamins,” Rine said. Because the human genome contains about 6 billion DNA base pairs, each one subject to mutation, there could be between 3 and 6 million DNA sequence differences between any two people. Given those numbers, he reasoned that, as in bacteria, “there should be people who are genetically different in terms of the amount of vitamin needed for optimal performance of their enzymes.”

This touches on what Rine considers one of the key biomedical questions today. “Now that we have the complete genome sequences of all the common model organisms, including humans, it’s obvious that the defining challenge of biology in the 21st century is not what the genes are, but what the variation in the genes does,” he said.

Rine, Marini and their colleagues are continuing to study variation in the human MTHFR gene as well as other folate utilizing enzymes, particularly with respect to how defects in these enzymes may lead to birth defects. Rine also is taking advantage of the 1,500 students in his Biology 1A lab course to investigate variants of a second vitamin B6-dependent enzyme, cystathionine beta-synthase.

He also is investigating how enzyme cofactors like vitamins and minerals fix defective enzymes. He suspects that supplements work by acting as chaperones to stabilize the proper folding of the enzyme, which is critical to its catalytic activity. “That is a new principle that may be applicable to drug design,” Rine said.


Article adapted by MD Only from original press release.
Contact: Robert Sanders
UC Berkley

Coauthors with Rine and Marini are UC Berkeley research assistant Jennifer Gin and Janet Ziegle, Kathryn Hunkapiller Keho, David Ginzinger and Dennis A. Gilbert of Applied Biosystems, which also funded part of the study. The work was supported by a University of California Discovery Grant, DARPA and the National Institutes of Health.

Increased intakes of folate intake can decrease male hearing loss risk by 20 percent, according to new research presented at the 2009 American Academy of Otolaryngology-Head and Neck Surgery Foundation (AAO-HNSF) Annual Meeting & OTO EXPO, in San Diego, CA.

The study, which identified 3,559 cases of men with hearing loss, found that there was no beneficial association with increased intakes of antioxidant vitamins such as C, E, and beta carotene. However, the authors found that men over the age of 60 who have a high intake of foods and supplement high in folates have a 20 percent decrease in risk of developing hearing loss.

Hearing loss is the most common sensory disorder in the United States, affecting more than 36 million people. High folate foods include leafy vegetables such as spinach, asparagus, turnip greens, lettuces, dried or fresh beans and peas, fortified cereal products, sunflower seeds and certain other fruits and vegetables are rich sources of folate. Baker’s yeast, liver and liver products also contain high amounts of folate.

The authors believe this is the largest study to delve prospectively into the relation between dietary intake and hearing loss. They used the most recent figures from the Health Professionals Follow-up Study cohort from years 1986 to 2004, a group consisting of 51,529 male health professionals. They were first enrolled into this study in 1986 and filled out detailed health and diet questionnaires every other year. The authors believe their findings can allow greater education, prevention, and screening efforts.


Article adapted by MD Only from original press release.


Contact: Matt Daigle
American Academy of Otolaryngology — Head and Neck Surgery

About the AAO-HNS

The American Academy of Otolaryngology – Head and Neck Surgery, one of the oldest medical associations in the nation, represents more than 12,000 physicians and allied health professionals who specialize in the diagnosis and treatment of disorders of the ears, nose, throat, and related structures of the head and neck. The Academy serves its members by facilitating the advancement of the science and art of medicine related to otolaryngology and by representing the specialty in governmental and socioeconomic issues. The organization’s vision: “Empowering otolaryngologist-head and neck surgeons to deliver the best patient care.”

Married men are healthier than men who were never married or whose marriages ended in divorce or widowhood, according to a major survey of American adults. Is marriage itself responsible for better health and longer life? It’s hard to be sure, but marriage certainly seems to deserve at least part of the credit, reports the July 2010 issue of Harvard Men’s Health Watch.

Numerous studies conducted over the past 150 years suggest that marriage is good for health. Now scientists are beginning to understand how marriage affects heart disease, cancer, and other conditions in men, says Harvard Men’s Health Watch.

A recent report from the Framingham Offspring Study notes that married men had a 46% lower rate of death than unmarried men, even after taking into account major cardiovascular risk factors. In this study, the happiness of the marriage did not seem to influence the overall protective effect. In other studies, though, marital unhappiness and stress were linked with high blood pressure (hypertension), an important cardiac risk factor. Over time, marital stress is associated with thickening of the left ventricle, the heart’s main pumping chamber. On the flip side, a supportive marriage is associated with improved survival among men who develop heart failure.

Marriage doesn’t appear to reduce the overall risk of getting cancer, but it may influence the outcome. One survey of people with cancer found that those who were unmarried were more likely to have advanced disease at the time of diagnosis than those who were married. Among those who receive cancer therapy, marriage has been linked to improved survival.

Read the full-length article: “Marriage and men’s health”