Craig Venter – Synthetic Cells

Deepak Chopra – Consciousness/Unconsciousness

John Mackey on Healthcare

Greg Lucier on Genomics



By Gabe Mirkin MD, July 29, 2011  —  When foods are cooked at temperatures above that of boiling water (100 C or 212F), sugar sticks to proteins and fats to form chemicals called Advanced Glycation End Products (AGEs).


Eating food cooked at high temperatures markedly elevates tissue,

blood and urine levels of AGEs to increase risk for; diseases of

inflammation such as cancers, arteriosclerosis, asthma, arthritis,

diabetes, Alzheimer’s Disease, heart attacks and strokes; damage

to the eyes and kidneys, and conditions such as cataracts, gum

infections, nerve damage and muscle injuries in athletes.


HOW AGEs FORM IN FOODS: When carbohydrates (chains of

sugars) are cooked with proteins or fats at high temperatures and

WITHOUT WATER, sugar binds to proteins or fats to form AGEs. When

carbohydrates are cooked in water, they do not attach to protein

and fat. Browning during cooking is a sign that AGEs are being

formed. AGEs are found in grilled, roasted, broiled, fried or

baked foods, and in coffee (made from roasted coffee beans).


YOUR BODY ALSO MAKES AGEs whenever your blood sugar level

rises too high.  This is most likely to happen when you eat sugary

foods and become inactive after eating.  A high rise in blood

sugar causes sugar to stick to cell membranes. Once there, sugar

cannot get off and eventually destroys the involved cells. Blood

sugar levels rise after you eat.  If you exercise just before or

after you eat, contracting muscles can draw sugar from the

bloodstream without even needing insulin.




  • Avoid foods that cause a high rise in blood sugar, such as

sugared drinks and foods with added sugars


  • Eat plenty of foods that do not cause a high rise in blood

sugars such as raw, streamed or simmered vegetables and fruits.


  • Restrict processed carbohydrates such as foods made from flour

(bakery products and pastas),


  • Use water-based cooking methods whenever possible: steaming,

simmering, blanching or boiling.  Water prevents the sugars from

attaching to proteins and fats.


  • Limit or avoid brown-cooked foods: those that are grilled,

broiled, roasted, fried or baked.


References: Am J Clin Nutr, June 2011;  Am J Clin Nutr. May 2010,

Neurobiol Aging, May 21, 2009;  J Gerontol A Biol Sci Med Sci Sept

2010.  Source:


Massive Project to Study the Link between Genetics and Health


Spit kit: Genetic data from a diverse group of 100,000 California patients will be gleaned from samples of saliva, captured in kits like this one.
Credit: Kaiser Permanente




Kaiser Permanente has compiled the genetic and medical data of 100,000 of its members



MIT Technology Review, July 27, 2011, by Emily Singer  —  Most health insurers are wary of genetics because, in most cases, it’s not yet clear how a particular genetic variation influences an individual’s health, or whether it should affect their care.

Now Kaiser Permanente, the nation’s largest nonprofit health plan, has announced that it’s finished the first phase of a massive project to compile genetic, medical, and environmental information for 100,000 of its members. Researchers also analyzed the length of participants’ telomeres—a molecule structure at the tip of the chromosome that has been linked to aging. This represents the largest telomere study to date.

The resulting data, gathered in collaboration with the University of California, San Francisco, will soon be available to outside researchers who study how different genetic and environmental factors influence disease. It took about 15 months for the team to collect and analyze the genomes of 100,000 people ranging in age from 18 to 107. The team used gene microarrays—small chips designed to quickly detect hundreds of thousands of genetic variations across the genome.

While genetic studies have been done on this scale before, they focused on one or a few diseases, such as diabetes and heart disease. The Kaiser project is unusual in that it includes years of comprehensive medical information—including blood-test results, medications, and other conditions—in the form of electronic health records. (Kaiser was one of the earliest adopters of electronic medical records in the United States.)

“The computerized data goes back 15 years,” says Neil Risch, a statistical geneticist at UCSF who co-led the study.  “It’s not like we have 100,000 blood-pressure measurements—it’s closer to a million.” By combining that information with prescriptions, for example, researchers could examine how genetics influence blood pressure and the effectiveness of medication.

Researchers will also incorporate environmental data, such as air-quality and water-quality records, based on knowledge of where participants lived and when.

Because the average age of the participants in the study is 65, “we think some of the most interesting initial questions will relate to aging,” says Cathy Schaefer, executive director of the Kaiser Permanente Program on Genes, Environment, and Health, and a co-leader on the project. “Specifically, are there genetic and environmental influences that lead to people living to a ripe old age without serious problems?”

Researchers will continue to follow participants as long as they continue to receive health care from Kaiser. They can examine, for example, how accurately telomere length can predict longevity or healthy aging.

Genetic studies such as these have often raised privacy issues—the concern is that individual participants could be identified and their data misused. In this case, because the health-plan provider is involved in the research, the fear is that Kaiser could use genetic information to alter rates or drop some members. But this type of discrimination is outlawed by the Genetic Information Non-Discrimination Act, passed in 2008. In addition, research participants’ information has special protection under the Health Insurance Portability and Accountability Act.

Patrick Taylor, a fellow at Harvard Law School’s Center for Health Law Policy, Biotechnology, and Bioethics, says he is not concerned about privacy issues in this case, in part because the project has oversight from the National Institutes of Health. (The project was funded by a two-year $24.8 million grant from the NIH.)  In addition, Kaiser has a long history of commitment to its members, says Taylor, who has studied the organization.

Bacteria blues: Bacteria collected in the bottom of the tube on the right have been labeled with a blue imaging agent.   Credit: Niren Murthy




A new contrast agent could detect bacteria on medical implants, and help doctors decide how to treat infection




MIT Technology Review, July 27, 2011, by Katherine Bourzac  —  A new contrast agent that targets microbes can be used to illuminate bacterial infections in living animals. It could ultimately enable doctors to safely spare more of a limb during amputations.

It’s usually clear when a patient has a bacterial infection and needs to be treated with antibiotics, says Jason Bowling, director of epidemiology at the University of Texas Health Science Center at San Antonio, who was not involved with developing the imaging agent. But sometimes an infection is more difficult to diagnose. For example, it can be difficult to tell when a patient who has pain at the site of a hip or knee replacement has an infection. This sometimes leads doctors to prescribe antibiotics when they aren’t necessary.

An imaging scan capable of detecting bacteria would quickly answer the question, sparing uninfected patients from unnecessary antibiotics or even from surgery to remove the implant. Where there is an infection and the implant is removed, imaging could help ensure that no new hardware is implanted until the infection has been completely cleared.

It’s challenging to image infections because many of the molecules used to target bacteria can accumulate in tissue that is merely inflamed rather than infected, says Niren Murthy, professor of biomedical engineering at Georgia Tech, who was involved with developing the new agent. The new imaging agent is taken up by bacteria in large quantities, but it won’t stick around in other tissue. “We had to find something very specific to bacteria,” he says.

Murthy’s group stole a trick from a group of viruses that gets its genome inside bacteria by attaching it to a bacterial food source, a carbohydrate called maltohexaose. Bacteria have proteins on their cell walls whose job is to bring maltohexaose inside the cell, and this happens even if that maltohexaose is attached to an imaging agent. Animal cells don’t have these proteins, so they don’t take up the contrast agent.


There are already two bacterial imaging agents on the market for use in preclinical research. But these are not as sensitive or as versatile as the Georgia Tech probe, says W. Matthew Leevy, professor of chemistry and director of biological imaging research at the University of Notre Dame. Those earlier imaging agents work by a different mechanism—they stick to bacterial cell walls rather than accumulate inside the cell. The Georgia Tech probe is two orders of magnitude more sensitive than any made in the past, which means it can detect much smaller populations of bacteria. Leevy says it should be compatible with a wide array of imaging technologies, including MRI, PET, and fluorescence imaging.

In a paper published online in the journal Nature Materials this week, Murthy describes imaging bacterial infections in living mice using the new contrast agent—maltohexaose attached to a fluorescent protein. Fluorescent imaging is useful for animal studies, but the method can’t be used to visualize the deep tissues of the body because the light simply cannot get out. Murthy is now coupling maltohexaose with imaging agents suitable for imaging with PET.

It will be critical to make the new contrast agent compatible with imaging technologies commonly found in hospitals, says Bowling, who runs a clinic where he monitors patients with bone infections. He says it’s often difficult to decide whether a patient has recovered and can be taken off the drugs. “There’s not a lot of data on when to stop treatment, and you can’t tell if you’ve truly cleared an infection or not,” he says. Other uses for the imaging agent might include helping doctors determine whether a diabetic’s foot problems are due to infection, and visualizing the extent of an infection in patients who need an amputation.

Leevy says he expects the agent to be available to researchers soon, but he says it could be difficult to bring the imaging technology into the clinic. While it could make a big difference for some patients, he says, the narrow potential market could discourage a company from making the large investment necessary to bring the agent through clinical trials.

New Type of Drug Kills Antibiotic-Resistant Bacteria


Nano killer: This drug-resistant staph bacterium has been split open and destroyed by an antimicrobial nanoparticle.   Credit: IBM




Scientists hope bacteria won’t develop resistance to nanoparticles that poke them open



MIT Technology Review, Spring/Summer 2011, by Katherine Bourzac  —  Researchers at IBM are designing nanoparticles that kill bacteria by poking holes in them. The scientists hope that the microbes are less likely to develop resistance to this type of drug, which means it could be used to combat the emerging problem of antibiotic resistance. This type of drug has not had much success in clinical trials in the past, but initial tests of the nanoparticles in animals are promising.

Drug-resistant bacteria have become a major problem. In 2005, nearly 95,000 people in the United States developed a life-threatening staph infection resistant to multiple antibiotics, according to the U.S. Centers for Disease Control and Prevention. It takes just one to two decades for microbes to develop resistance to traditional antibiotics that target a particular metabolic pathway inside the cell, says Mary B. Chan-Park, professor of chemical and biological engineering at Nanyang Technological University in Singapore, who was not involved with the research. In contrast, drugs that compromise microbes’ cell membranes are believed to be less likely, or slower, to evoke resistance, she says.

“We’re trying to generate polymers that interact with microbes in a very different way than traditional antibiotics,” says James Hedrick, a materials scientist at IBM’s Almaden Lab in San Jose, California. To do this, Hedrick’s research group took advantage of past work on a library of polymer building blocks that can be mixed and matched to make complex nanoparticles. To make a nanoparticle that would selectively attack bacterial membranes and then break down harmlessly inside the body, the IBM group put together three types of building blocks. At the center of the polymer sequence is a backbone element that’s water-soluble and tailored to interact with bacterial membranes. At either end of the backbone is a hydrophobic sequence. When a small amount of these polymer chains are added to water, the differences between the ends and the middle of the sequence drive the polymers to self-assemble into spherical nanoparticles whose shell is entirely made up of the part that will interact with bacterial cells. This work is described this week in the journal Nature Chemistry.

IBM’s labs aren’t equipped for biological tests, so the researchers collaborated with Yi Yan Yang at the Singapore Institute of Bioengineering and Nanotechnology to test the nanoparticles. They found that the nanoparticles could burst open and kill gram-positive bacteria, a large class of microbes that includes drug-resistant staph. The nanoparticles also killed fungi. Other types of deadly bacteria that have different types of cell membranes would not be vulnerable to these nanoparticles, but the IBM researchers say they are developing nanoparticles that can target these bacteria, too, though it is more difficult. “Through molecular tailoring,” says Robert Allen, senior manager of materials chemistry at IBM Almaden, “we can do all sorts of things”—designing particles with a particular shape, charge, water solubility, or other property.

The IBM researchers believe the drug could be injected intravenously to treat people with life-threatening infections. Or it could be made into a gel that could be applied to wounds to treat or prevent infection.

However, Chan-Park cautions, other drugs that work by this membrane-piercing mechanism have not been very successful so far. Those that have shown early promise on the lab bench either were toxic to animal cells or simply didn’t work in the complex environment of the human body.

More tests will be needed to say definitively whether the nanoparticles are safe and will work in people. Initial tests of the IBM particles with human blood cells and in live mice have been promising. Allen says the nanoparticles didn’t interact with human blood cells because their electrical charge is significantly greater than that of bacterial cells. There were no signs of toxicity in mice injected with the particles, and none of them died.

In addition to developing nanoparticles that can attack other types of bacteria, the IBM group is working on making larger quantities of the designer polymers, scaling up from the current two-gram capacity to the kilogram quantities needed for larger clinical tests. IBM won’t be getting into the pharmaceutical business, says Allen, but the company plans to partner with a healthcare company to license the polymer drugs.


A migraine is a headache with throbbing pain that is usually worse on one side of the head. The pain is often severe enough to hamper daily activities and may last from four hours to three days if untreated. More than one in 10 Americans, including one in 6 women, have migraines, but many have been told mistakenly that they have a sinus or tension headache. Foods, stress, and hormones can be migraine triggers.

About 20% of people who suffer from migraines will have an aura about 20 minutes to an hour before the pain. They may see flashing lights, wavy lines, or dots, or they may have blurry vision or blind spots. These are called “classic migraines.”



Throbbing pain typically occurs on one side near the temples, forehead, and eyes. Migraines can make you very sensitive to light, sound, or mild exertion, such as climbing the stairs. Many people have nausea, vomiting, or vision problems. The pain can be disabling, forcing people to miss work or other activities.

Some people may have a change in mood before a migraine begins. They may become more excitable or irritable or depressed. Others may detect a sensation, such as a funny smell or taste. They may feel more fatigued, yawn frequently, or experience muscle tension. About 1 in 4 people experience this prodrome phase, which can occur as early as 24 hours before any head pain.



Migraines may be set off by some specific cause, such as flickering lights. This could be a reflection from snow or water or from fluorescent bulbs or television or movie screens. Wearing polarizing sunglasses outside and using daylight spectrum fluorescent bulbs inside may help.




An Advantage of Aging

Migraines most often strike in the prime of life – between the ages of 20 and 60. While elderly people still get migraines, they often decrease in severity and frequency as we age, or even disappear entirely. Good management of migraines may help you get rid of your migraines for good.




Migraine Miseries Push Patients to Ways of Coping



Graphic: Stuart Bradford




The New York Times, July 26, 2011, by Tara Parker-Pope  —  The news that the presidential candidate Michele Bachmann suffers from severe migraines has touched off a national discussion about a surprisingly common disorder that is little understood and often undertreated.

Migraine patients are coming forward with their stories. And while each one is different, they have two common threads: suffering and trying to cope.

For some, a migraine represents throbbing head pain and nausea so severe they retreat to a darkened room for a day or more. For others, it’s about a scary moment, driving on the highway when a migraine-induced aura or vision change forces them to pull over.

“Imagine someone having driven a nail straight through your head,” said Craig Partridge, 50, chief scientist for a high-tech research company in East Lansing, Mich., who began having migraines in his late teens. “And then they periodically tap on it to remind you it’s there. It’s that painful.”

More than 10 percent of adults and children suffer from migraine — which is three times as common in women and girls as in men and boys — and the Migraine Research Foundation reports that nearly a quarter of households are affected. The World Health Organization ranks migraine among the top 20 most debilitating health conditions; more than 90 percent of sufferers are unable to work or function normally during an attack, which can last for hours or even days.

Some migraine sufferers say the attacks are so debilitating they couldn’t imagine taking on a job with significant responsibility. But others note that years of experience and new drug treatments have helped them find ways to cope. Some say the condition forced them to take better care of themselves and adopt healthful behaviors, like getting enough sleep and learning to manage stress.

Mr. Partridge has learned to avoid caffeine and bright lights, and is vigilant about wearing sunglasses in strong sunlight. Years of taking ibuprofen to treat headaches led to an ulcer. Eventually, he learned that a magnesium supplement reduced the frequency of his headaches, and now he gets only about three a year.

“As far as I can tell, everyone is a little different,” he said. “Some people have auras, but I never had auras. I get tunnel vision. My tongue starts to get heavy and I have trouble talking.”

Kat Smith, a 47-year-old mother of three in Bryn Mawr, Pa., remembers her teenage brother suffering terribly from migraines, but she never experienced them until a bike accident in her 20s. Then, after the birth of her son, she had migraines “regularly and fiercely” about 12 times a month. She discovered that small amounts of alcohol and vigorous physical activity acted as a trigger.

“I was a fairly carefree person, but I became rigid, very disciplined with myself,” she said. “It seemed I had to eliminate things that other people associated with joy. I had to reconstruct my life as a person of migraine after accepting that these weren’t going to go away.”

She adapted, giving up ice hockey and aerobics and switching to yoga. But sometimes she pushes her limits. This weekend she took part in a vigorous dance class and was punished with a migraine.

“I’ll do something incredibly vigorous and physical, and it will feel so good,” she said. “That night I will get a massive migraine.”

For many patients, including Ms. Smith, a class of migraine drugs called triptans have been a godsend, helping to cut short the pain. Triptans work by causing blood vessels in the brain to constrict and change blood flow, and can often stop a migraine completely or reduce its severity if taken in the early minutes of an attack.

Other patients take daily treatments to prevent migraine from setting in. Barbara Thompson, a 59-year-old communications specialist in Manhattan, uses Topamax, a seizure drug that has been shown to prevent migraine. An attack sometimes “breaks through” despite the daily dose, and on those days she uses a triptan drug.

“Often I get them when I’m at work,” she said. “I find that I get more quiet, and I have to focus more intently on what I’m doing. It’s a more internal day — I don’t have a better way of putting it.”

In a video that went viral, the television reporter Serene Branson babbled gibberish last winter during a live report from the Grammy Awards. At first, it seemed as if she were having a stroke on live television, but her doctor later concluded that a complex migraine had rendered her unable to form words.

Some migraine sufferers, including Ms. Bachmann, experience pain so severe they go the emergency room. But a recent review of emergency room doctors in Ontario found that patients were rarely treated with the proper drugs for migraine, according to a report last month in the journal Pain Research & Management.

The data suggests that more education is needed.

“If it’s not well controlled with the right combination of preventative or acute therapy, it can be very disabling,” said Dr. Satnam Nijjar, the study’s lead author and an assistant professor of neurology at the Johns Hopkins Headache Center. “It’s probably the most common cause for time missed from work in the U.S.”

Robert Dalton, executive director of the National Headache Foundation in Chicago, says that while migraines can be impairing, the larger problem is that many sufferers aren’t getting proper medical care.

“What we want to make sure people understand,” he said, “is that it’s a debilitating disease when it’s not managed properly.”



Alternative Therapy: Biofeedback

Biofeedback and relaxation training can give you relief that is similar to the help you get from medications. Biofeedback uses a monitor to train you to recognize the onset of muscle tension and changes in body temperature that are signals of stress.




Lung Cancer Slowed by First-Line EGFR Inhibition

By Charles Bankhead, Staff Writer, MedPage Today

Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner




July 26, 2011  —  Patients with advanced lung cancer had a threefold improvement in progression-free survival with first-line erlotinib (Tarceva) instead of chemotherapy, final results of a randomized trial showed.


The erlotinib group had a median progression-free survival of 13.1 months versus 4.6 months for those treated with a standard chemotherapy doublet. The difference represented an 84% reduction in the hazard for progression or death, Chinese investigators reported online in The Lancet Oncology.


The results constitute “conclusive evidence that erlotinib provides superior overall response rate and progression-free survival versus platinum doublet-chemotherapy as first-line treatment in Asian patients whose tumors harbor activating mutations of epidermal growth factor receptor (EGFR),” Caicun Zhou, MD, of Tongji University in Shanghai, and co-authors wrote in conclusion., “The results of this study have practice-changing implications and provide justification for widespread implementation of routine EGFR mutation testing in advanced non-small cell lung cancer (NSCLC).”

The findings corroborate the initial report last year at the European Society for Medical Oncology meeting.

EGFR mutations occur in a substantial proportion of NSCLC tumors, ranging from about 8% in white populations to 30% of Asian patients (N Engl J Med 2009; 361: 947-957, J Natl Cancer Inst 2005; 97: 339-346, J Thorac Oncol 2007; 2: 430-439).

The frequency of EGFR-mutant tumors provided a rationale for treatment with EGFR inhibitors, which include erlotinib. The rationale was borne out in a phase III trial that demonstrated improved overall survival with erlotinib in patients with previously treated NSCLC (N Engl J Med 2005; 353: 123-132).

Whether EGFR inhibition offered a survival benefit as first-line therapy was the question posed by Zhou and co-investigators in the OPTIMAL trial, conducted at 22 centers in China.

Eligible patients had newly diagnosed stage IIIB-IV NSCLC with confirmed activating mutations in EGFR.

Patients were randomized to first-line chemotherapy with gemcitabine and carboplatin or to erlotinib.

Patients in the chemotherapy arm received a maximum of four cycles of therapy. Those randomized to erlotinib continued treatment until disease progression, development of unacceptable toxicity, or withdrawal from the study.

Investigators screened 549 patients and randomized 165. The final analysis involved 82 patients in the erlotinib arm and 72 in the chemotherapy arm. The primary endpoint was progression-free survival.

When the trial ended, the erlotinib group had an 8.5-month improvement in progression-free survival, which translated into a hazard ratio of 0.16 versus chemotherapy (P<0.0001).

Erlotinib was also associated with a more favorable safety profile.

Grade 3-4 toxicity in the chemotherapy arm included neutropenia in 30 patients (42%) and thrombocytopenia in 29 (40%); none of the patients in the erlotinib arm developed neutropenia or thrombocytopenia.

The most common grade 3-4 toxicity with erlotinib was elevated alanine aminotransferase (in three patients) and skin rash (in two).

Serious adverse events occurred in 10 patients (14%) in the chemotherapy arm versus two (2%) in the erlotinib group.

Similar trials involving the EGFR inhibitor gefitinib (Iressa) resulted in a median progression-free survival of 10.4 and 9.2 months.

Given those results, the median progression-free survival of 13.1 months with erlotinib “is amazing,” Tetsuya Mitsudomi, MD, of Aichi Cancer Center Hospital in Nagoya, Japan, wrote in an accompanying commentary.

Although no trial of first-line EGFR inhibition in NSCLC has demonstrated a benefit in overall survival, “failure to translate extended progression-free survival into increased overall survival is accounted for by the substantial crossover of treatment after progression of disease,” Mitsudomi wrote.

“Yet, this crossover should not lead to underestimation of the power of EGFR tyrosine kinase inhibitors (TKIs) in patients with EGFR mutations.”

“EGFR TKIs are undoubtedly key drugs for patients with EGFR mutations and should be used early in treatment,” he added. “However, when EGFR test results cannot be obtained in a reasonably short time frame, first-line chemotherapy and second-line EGFR TKI after progression is a reasonable option if the patient is later shown to be EGFR mutation-positive.”

Preliminary data from a randomized European trial has also demonstrated a significant progression-free survival advantage in favor of first-line erlotinib versus chemotherapy in patients with EGFR-positive tumors.

The OPTIMAL trial was supported by F Hoffmann-La Roche China and the Science and Technology Commission of Shanghai Municipality.

Zhou disclosed relationships with Roche, Roche China, and Eli Lilly China. Co-author Yi-Long Wu disclosed relationships with Roche, Eli Lilly, Pfizer, and AstraZeneca. Co-author Jie Wang disclosed relationships with AstraZeneca, Eli Lilly, and Roche. Co-author Li Zhang disclosed relationships with Lilly, AstraZeneca, and Roche.

Mitsudomi disclosed relationships with Pfizer, Boehringer Ingelheim, Chugai Pharmaceuticals, Eli Lilly, and AstraZeneca.

Primary source: The Lancet Oncology
Source reference:
Zhou C, et al “Erlotinib versus chemotherapy as first-line treatment for patients with advanced EGFR mutation-positive non-small cell lung cancer (OPTIMAL, CTONG-0802): A multicenter, open-label, randomized, phase III study” Lancet Oncol 2011; DOI: 10.1016/S1470-2045(11)70184-X.

Additional source: The Lancet Oncology
Source reference:
Mitsudomi T “Erlotinib, gefitinib, or chemotherapy for EGFR mutation-positive lung cancer?” Lancet Oncol 2011; DOI: 10.1016/S1470-2045(11)70194-2.


By Gabe Mirkin MD

July 25, 2011

A study From Harvard School of Public Health shows that telling overweight people to “eat less and exercise more” rarely helps them lose weight (New England Journal of Medicine, June 23, 2011). That encourages them to eat any foods they want and, as they age, they continue to gain weight which is associated with increased risk for heart disease, diabetes, strokes, breast cancer, colon cancer, and premature death.

120,877 healthy, non-obese women and men were followed for 20 years. The study shows which foods and lifestyle factors should be avoided to prevent an average weight gain of almost 17 pounds in 20 years. If you eat the wrong foods, you can gain weight even if you exercise. Small changes in eating and exercising can prevent this weight gain. Those who were overweight at the start of the study gained the most weight over the study time.

Study surprises: Weight gain is not associated with eating yogurt, nuts, or peanut butter. Yogurt appears to contain bacteria that cause the body to produce hormones that make you less hungry. Nuts contain primarily monounsaturated fats that are not associated with increased risk for weight gain.

Foods that caused the most weight gain:
• French fries (2 lbs per four-year period)
• potato chips (1.69 lbs)
• potatoes (1.28 lbs)
• other forms of potatoes (0.57 lb)
• sugar-sweetened beverages (1 lb)
• red meats (0.95 lb)
• processed meats (0.93 lb)
• refined grains (0.39 lb)
• sweets and desserts (0.41 lb)
• other fried foods (0.32 lb)
• fruit juice (0.31 lb)
• butter (0.3 lb)

Foods that caused weight loss:
• vegetables (-0.22 lb per four-year period)
• whole grains (-0.37 lb)
• fruits (-0.49 lb)
• nuts (-0.57 lb)
• yogurt (-0.82 lb).

Lifestyle factors: In addition to diet, the study shows that you should exercise daily, sleep 6 to 8 hours a day, restrict television watching, avoid smoking and do not take more than one drink a day.



Can you predict which children are likely to excel in certain sports just by looking at them?

Yes! Those with the longest Achilles tendons in the back of the lower leg will probably be better long distance runners, while those with the shortest Achilles tendons will probably be the best body builders (Medicine & Science in Sports & Exercise, August 2011) .

Look at the ratio of the Achilles tendon to the large bulge above it which is the calf muscle group. If the Achilles tendon is more than half way up your leg, you have a long tendon and have an advantage in running long distances. If the calf muscle bulge goes down almost to your ankle, you have the potential to be a body builder. Body building contests require athletes to have very large muscles which are characterized by long muscles with shorter tendons.

When you run, you land on your foot and spring forward in the air to drive your body forward. When you land, the Achilles tendon stretches and stores up to 70 percent of the energy of the force of your foot hitting the ground. Then the tendon shortens to release this extra stored energy, to drive you forward. Those with the longest tendons store the most energy to drive you forward with greater force. The authors proved this by showing that people with longer Achilles tendons required less oxygen to drive them forward after their foot hits the ground. Lack of oxygen is the limiting factor to how fast you can run over long distances.



Why have I suffered sports injuries primarily in the winter and spring?

You could lack vitamin D. To meet your needs for that vitamin, you have to expose your skin to sunlight or take vitamin D pills. You cannot get enough vitamin D from foods.

NFL players with low vitamin D levels are at increased risk for muscle and tendon injuries (American Orthopaedic Society for Sports Medicine’s Annual Meeting in San Diego, July 11, 2011). The lower the level of vitamin D, the more likely the players were to be injured.

Vitamin D acts directly on specific receptors in muscles to make them stronger and prevent injury (Scandinavian Journal of Medicine & Science in Sports, April 2010). A review of several studies shows that giving vitamin D pills to athletes with normal blood levels may not strengthen muscles, but lack of vitamin D weakens muscles. Giving athletes who have a deficiency defined by blood levels of D3 below 25 nmol/L, strengthens their muscles (Osteoporosis International, October, 2010).

We have known for more than 50 years that taking large doses of male hormones can help athletes recover faster and grow stronger with significantly larger muscles. Recent research shows that male hormones (the anabolic steroid nandrolone decanoate) strengthens muscles by stimulating the vitamin D receptor in muscles (Annual Meeting of the Endocrine Society, June, 2011). Athletes with vitamin D3 levels below 75 nmol/L may need more sunlight or vitamin D pills.



Lifting Weights Makes Bones Stronger

By Gabe Mirkin, M.D., July 25, 2011  —   An interesting study from the University of British Columbia showed that lifting weights strengthens the bones of women in their late sixties. The women were asked to use several weight machines three times a week for one year. At the end of that year, the women gained a tremendous amount of muscle strength, and they also had denser bones.

If a woman lives long enough, she will certainly develop osteoporosis which can shorten her life. This study shows that it is never too late to strengthen bones. If she already has osteoporosis, her doctor may advise bone-strengthening drugs such as Fosamax or calcitonin. Whether or not she takes drugs or supplements, she should start an weight-lifting exercise program. Join a gym that has weight-training machines and pick six to ten of the machines. Do a set of eight movements in a row on the first machine, rest a few seconds and then do two more sets of eight. Do this on each of the machines. Repeat this routine two or three times a week. It’s never too late to start.

EC Rhodes, AD Martin, JE Taunton, M Donnelly, J Warren, J Elliot. Effects of one year of resistance training on the relation between muscular strength and bone density in elderly women. British Journal of Sports Medicine, 2000, Vol 34, Iss 1, pp 18-22.



Flat Feet are Good For You

By Gabe Mirkin, M.D., July 25, 2011People with flat feet usually can run fast and are less likely to become injured. During World War II, having flat feet would have kept you out of the army, but a study published in the Archives of Family Medicine shows that army recruits who have the flattest feet suffer the fewest injuries.

Healthy army recruits had their arches measured before they started 12 weeks of basic training. Those with the flattest feet had the fewest injuries. When you run, you land on the outside bottom of your feet and roll inward to absorb the hard shock of your foot striking the ground. Most people who have flat feet have normal arches. Their feet appear flat because they have flexible ankles that allow their feet to roll so far inward that their arches touch the ground, so you can’t see them. The more you roll in, the greater the shock absorption and protection from injury. People with flat feet also are often fast runners because rolling in allows their feet to press harder on the ground to force them forward with greater force.



How to Raise Good HDL Cholesterol




By Gabe Mirkin MD, July 25, 2011  —  If your good HDL cholesterol is below 35, you are at increased risk for heart attacks. You can reduce chances of suffering a heart attack by two percent for every mg/dl rise in HDL.

To raise HDL cholesterol, burn at least 1200 calories with exercise per week. Lose weight if you are overweight. For every pound of fat lost, expect a one percent rise in HDL (1).

Exercise before you eat fat. A study at the University of Missouri showed that exercising regularly before eating high-fat meals raises HDL cholesterol considerably (2). Exercise stimulates the fat-clearing enzyme, lipoprotein lipase, which drops triglycerides to produce more HDL cholesterol.

Don’t smoke. A study at Vanderbilt University showed that within just one week of quitting smoking, HDL levels increased by seven points.

Avoid refined carbohydrates — sugar, flour, white rice and milled corn. Foods that cause a spike in blood sugar drop your HDL cholesterol.

1)                       Peter Kokkinos, a clinical exercise physiologist at Georgetown University observed the effect in 3,000 men. Tom Thomas, at the U of Missouri. Checked 4/14/11





Glucosamine and Chondroitin Sulfate for Arthritic Pain



By Gabe Mirkin, M.D., July 25, 2011  —  One in 10 Americans suffers from osteo or degenerative arthritis, a disease in which the currently used medications, acetaminophen, aspirin and nonsteroidal antiinflammatory drugs, do not slow or reverse the progressive destruction of joints and no cause is known. Over the last decade, reports have shown that pills containing chondroitin sulfate and glucosamine, two components of cartilage, may help alleviate the pain. Three major reviews in the scientific literature claim that the three studies showing that glucosamine relieves pain were poorly designed and therefore cannot be offered as proof of benefit. On the other hand, six studies from Europe and another from the United States show that chondroitin sulfate does help to slow joint destruction and pain caused by osteoarthritis (journal references for these studies).

One study in Rheumatology showed that glucosamine is not more effective than a placebo in controlling arthritic pain (8).

Several studies show that glucosamine helps control pain, but it is very difficult to test the effect of any drug on pain because a very significant number of people will benefit just as much from placebos. The authors performed a double blind study over six months in which they gave either 1500 mg glucosamine or placebo pills daily to patients with arthritis. Neither the doctors nor the patients knew who received glucosamine. One out of three patients receiving glucosamine had excellent control of their pain. but one out of three people receiving placebos also had the same excellent response.

Another study in the British medical journal, Lancet, showed that glucosamine helps to retard the breakdown of cartilage. Up to then, studies showed only that glucosamine helps to relieve pain. People with arthritis received either 1500 mg of glucosamine or placebo. X rays of their knees showed that the placebo group lost more distance between the bones of their knees than the glucosamine group.

The ends of bones at the knee joint are covered with cartilage, so the greater the distance between the bones on X ray, the greater the amount of cartilage. There is a serious problem with the study. People with arthritis often cannot fully straighten their knees, so it is impossible to use distance between bones to determine how much cartilage is lost. For example, if a person bends his knees a little, he will have the bones closer together than when he holds his knees straight. That means that anything that blocks pain will allow person to straighten his knees and have a greater distance between the bones at the knee. You should get the same benefit from any pain medicine. Furthermore, the study was sponsored by Rotta Research Group, who could gain billions of dollars from sales promoted by this study.

An earlier editorial in Lancet raises questions about the safety of glucosamine (2). Most research shows that glucosamine can help to relieve some of the pain associated with arthritis (3), but does not help to prevent cartilaginous damage and has not been shown to heal broken cartilage. Therefore, it is no more effective in treating arthritis than aspirin, but costs more than aspirin, but less than most brand name arthritis pain drugs that your doctor prescribes.

Glucosamine helps form aggrecan, the part of cartilage that allows cartilage to swell and shrink, acting like a shock absorber to help protect your knees from the trauma of running and walking. Adding glucosamine to cartilaginous cells in a test tube causes them to increases production of aggrecan (4).

However, in light of this good news, you should know that glucosamine can block the effects of insulin, causing blood sugar levels to rise (5,6,7), increasing likelihood of suffering the side effects of diabetes in susceptible people.

1) Lancet, January 27, 2001

2 )Mark Adams: editorial The Lancet, July 31, 1999, 354(9176):353-354.

3) Muller-Fabbender et al. Glucosamine compared to ibuprofen in osteoarthritis of the knee. Osteoarthritis Cartilage. 1994;2:61-69.

4)Bassler et al. Stimulation of Proteoglycan production by glucosamine sulfate in chondrocytes isolated from human osteoarthritis articular cartilage in vitro. Osteoarthritis Cartilage. 1998;6:427-434.

5) Am J Physiol Cell Physiol 1996;270:C803-11.

6) Diabetes 1995;45:1003-10089.

7) Proc Assoc Am Phys 1998;110:422-432.

8) A randomized, double-blind, placebo-controlled trial of glucosamine sulphate as an analgesic in osteoarthritis of the knee. Rheumatology, 2002, Vol 41, Iss 3, pp 279-284. R Hughes, A Carr. Hughes R, Ashford & St Peters Hosp Trust, Dept Rheumatol, Guildford Rd, Surrey KY16 0PZ, ENGLAND

Source of all articles:

A Must Webinar: eSource and the Paperless Clinical Trial



Target Health is pleased to announce that Dr. Jules T. Mitchel will be running a Webinar, sponsored by FDANEWS, on the topic of “eSource and the Paperless Clinical Trial.“ The 90 minute Webinar will take place this Tuesday at 1:30.


Finally, in the clinical trial arena, the the R. Buckminster Fuller mantra of “doing more with less“ has arrived. Less paper equals more productivity, reduced time to the market and a greener world. If you’re looking to decrease onsite monitoring, decrease data entry transcription errors, decrease time to database lock, etc. now is your chance to learn how. Here are just a few of the specifics of the Webinar:


  • Source records: What they are, and the FDA’s perspective
  • Complying with FDA’s proposal for direct data entry
  • Paper backups for electronic records – the risks and the rewards
  • Impact of direct data entry on clinical research and data management
  • Paradigm shift: Product development and direct data entry
  • Impact of companies providing monitoring, data management and EDC services
  • And much more

For more information about Target Health contact Warren Pearlson (212-681-2100 ext. 104). For additional information about software tools for paperless clinical trials, please also feel free to contact Dr. Jules T. Mitchel or Ms. Joyce Hays. The Target Health software tools are designed to partner with both CROs and Sponsors. Please visit the Target Health Website,

Over Half of Alzheimer’s Cases May Be Preventable



Scientists can see the terrible effects of Alzheimer’s disease (AD) when they look at brain tissue under the microscope. AD tissue has many fewer 1) ___ cells and synapses than a healthy brain. Plaques, abnormal clusters of 2) ___ fragments, build up between nerve cells. Dead and dying nerve cells contain tangles, which are made up of twisted strands of another protein.


Plaques form when protein pieces called beta-amyloid  clump together. Beta-amyloid comes from a larger protein found in the fatty membrane surrounding nerve cells. Beta-amyloid is chemically “sticky“ and gradually builds up into plaques. The most damaging form of beta-amyloid may be groups of a few pieces rather than the plaques themselves. The small clumps may block cell-to-cell signaling at 3) ___. They may also activate immune system cells that trigger inflammation and devour disabled cells



Tangles destroy a vital cell transport system made of proteins. This electron microscope picture shows a cell with some healthy areas and other areas where 4) ___ are forming.



Over half of all AD cases could potentially be prevented through lifestyle changes and treatment or prevention of chronic medical conditions, according to a study led by Deborah Barnes, PhD, a mental health researcher at the San Francisco VA Medical Center. Analyzing data from studies around the world involving hundreds of thousands of participants, Barnes concluded that worldwide, the biggest modifiable risk factors for AD are, in descending order of magnitude, low 5) ___, smoking, physical inactivity, depression, mid-life hypertension, diabetes and mid-life obesity. In the United States, Barnes found that the biggest modifiable risk factors are physical 6) ___, depression, smoking, mid-life hypertension, mid-life obesity, low education and diabetes. Together, these risk factors are associated with up to 51%of AD cases worldwide (17.2 million cases) and up to 54% of Alzheimer’s cases in the United States (2.9 million cases), according to Barnes.


“What’s exciting is that this suggests that some very simple lifestyle changes, such as increasing 7) ___ activity and quitting smoking, could have a tremendous impact on preventing AD and other dementias in the US and worldwide,“ said Barnes, who is also an associate professor of psychiatry at the University of California, San Francisco. The study results were presented at the 2011 meeting of the Alzheimer’s Association International Conference on Alzheimer’s Disease in Paris, France, and published online on July 19, 2011 in Lancet Neurology.


Barnes cautioned that her conclusions are based on the assumption that there is a 8) ___ association between each risk factor and AD. “We are assuming that when you change the risk factor, then you change the 9) ___,“ Barnes said. “What we need to do now is figure out whether that assumption is correct.“ Senior investigator Kristine Yaffe, MD, chief of geriatric psychiatry at SFVAMC, noted that the number of people with Alzheimer’s disease is expected to 10) ___ over the next 40 years. “It would be extremely significant if we could find out how to prevent even some of those cases,“ said Yaffe, who is also a professor of psychiatry, neurology and epidemiology at UCSF.


ANSWERS 1) nerve; 2) protein; 3) synapses; 4) tangles; 5) education; 6) inactivity; 7) physical; 8) causal; 9) risk; 10) triple

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