What would happen if you centered your diet around vegetables, the most nutrient-dense food group?
“The plant-based nature of the diet may trump the caloric restriction, though, since the one population that lives even longer than the Okinawa Japanese don’t just eat a 98% meat-free diet, they eat 100% meat-free. The Adventist vegetarians in California, with perhaps the highest life expectancy of any formally described population.”
A very fascinating study shows that higher amounts of purpose in life correlate with lower interleukin-6 (= pro-inflammatory cytokine) levels. In addition it reveals that educational degrees stop playing a relevant role as soon as a certain amount of purpose in life is reached.
I’d be curious to hear if anyone experiences similar results. Even if the study was just a fluke, Nuts May Help Prevent Death by improving the function of our arteries (Walnuts and Artery Function) and fighting cancer (Which Nut Fights Cancer?) and inflammation (Fighting Inflammation in a Nut Shell).
Even eating nuts every day does not appear to result in expected weight gain (Nuts and Obesity: The Weight of Evidence), so enjoy!
Nick Wilkins was diagnosed with leukemia when he was 4 years old, and when the cancer kept bouncing back, impervious to all the different treatments the doctors tried, his father sat him down for a talk.
John Wilkins explained to Nick, who was by then 14, that doctors had tried chemotherapy, radiation, even a bone marrow transplant from his sister.
“I explained to him that we’re running out of options,” Wilkins remembers telling his son.
Curcumin and Knee Osteoarthritis
One hundred and seven patients with primary osteoarthritis of the knee were studied, including those with knee pain on a scale of 5 to 10 in intensity; radiographic osteophytes; and at least one of the following features: age >50, morning stiffness <30 minutes in duration, and crepitus on motion. The majority of the individuals were overweight women with a BMI >25. Participants were asked to discontinue their knee pain medications and were randomized to either ibuprofen 400 mg twice daily or Curcuma domestica extract, 500 mg four times daily for 6 weeks. Continue reading →
Researchers have found in a study done on mice that breathing motor vehicle emissions triggers a change in high-density lipoprotein (HDL) cholesterol, altering its cardiovascular protective qualities so that it actually contributes t o clogged arteries.
In addition to changing HDL from “good” to “bad,” the inhalation of emissions activates other components of oxidation, the early cell and tissue damage that causes inflammation, leading to hardening of the arteries, according to the research team, which included scientists from UCLA and other institutions.
Left: In fat tissue from a lean mouse, neutrophil elastase and a1-antitrypsin levels are balanced. Right: In fat tissue from an obese mouse, they are imbalanced — neutrophil elastase levels are high (dark staining) and a1-antitrypsin levels are low. (Credit: Sanford-Burnham Medical Research Institute)
Apr. 2, 2013 — Many recent studies have suggested
that obesity is associated with chronic inflammation in fat tissues. Researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) have discovered that an imbalance between an enzyme called neutrophil elastase and its inhibitor causes inflammation, obesity, insulin resistance, and fatty liver disease. This enzyme is produced by white blood cells called neutrophils, which play an important role in the body’s immune defense against bacteria. The researchers found that obese humans and mice have increased neutrophil elastase activity and decreased levels of α1-antitrypsin, a protein that inhibits the elastase. When the team reversed this imbalance in a mouse model and fed them a high-fat diet, the mice were resistant to body weight gain, insulin resistance (a precursor to type 2 diabetes), and fatty liver disease. Their study appears April 2 inCell Metabolism.
What happens when you reduce neutrophil elastase levels“The imbalance between neutrophil elastase and its inhibitor, α1-antitrypsin, is likely an important contributing factor in the development of obesity, inflammation, and other health problems. Shifting this balance — by either reducing one or increasing the other — could provide a new therapeutic approach to preventing and treating obesity and several obesity-related conditions,” said Zhen Jiang, Ph.D., assistant professor in Sanford-Burnham’s Diabetes and Obesity Research Center at Lake Nona, Orlando and senior author of the study.
This study began when Jiang and his team noticed that neutrophil elastase levels are particularly high and α1-antitrypsin levels are low in a mouse model of obesity. Then they saw the same thing in blood samples from human male volunteers.
To further probe this curious neutrophil elastase-obesity relationship, the researcher turned once again to mouse models. They found that mice completely lacking the neutrophil elastase enzyme don’t get as fat as normal mice, even when fed a high-fat diet. Those mice were also protected against inflammation, insulin resistance, and fatty liver. The same was true in a mouse model genetically modified to produce human α1-antitrypsin, which inhibits neutrophil elastase.
Normal mice on a high-fat diet were also protected against inflammation, insulin resistance, and fatty liver when they were given a chemical compound that inhibits neutrophil elastase. This finding helps validate the team’s conclusions about neutrophil elastase’s role in inflammation and metabolism and also suggests that a medicinal drug could someday be developed to target this enzyme.
Mechanism: how neutrophil elastase influences inflammation and metabolism
How do high neutrophil elastase levels increase inflammation and cause weight gain and other metabolic problems?
Jiang and his team began connecting the mechanistic dots. They discovered that neutrophil elastase-deficient mice have increased levels of several factors, including adiponectin, AMPK, and fatty acid oxidation. These are known for their roles in increasing energy expenditure, thus helping the body burn excess fat.
Virginie Mansuy-Aubert, Qiong L. Zhou, Xiangyang Xie, Zhenwei Gong, Jun-Yuan Huang, Abdul R. Khan, Gregory Aubert, Karla Candelaria, Shantele Thomas, Dong-Ju Shin, Sarah Booth, Shahid M. Baig, Ahmed Bilal, Daehee Hwang, Hui Zhang, Robin Lovell-Badge, Steven R. Smith, Fazli R. Awan, Zhen Y. Jiang. Imbalance between Neutrophil Elastase and its Inhibitor α1-Antitrypsin in Obesity Alters Insulin Sensitivity, Inflammation, and Energy Expenditure. Cell Metabolism, 2013; 17 (4): 534 DOI:10.1016/j.cmet.2013.03.005