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A positive association of lumbar spine bone mineral density with dietary protein is suppressed by a negative association with protein sulfur. Thorpe M, Mojtahedi MC, Chapman-Novakofski K, McAuley E, Evans EM. J Nutr. 2008 Jan;138(1):80-5. PMID: 18156408 Results suggest that protein intake is positively associated with aBMD, but benefit at the LS is offset by a negative impact of the protein sulfur acid load. If validated experimentally, these findings harmonize conflicting theories on the role of dietary protein in bone health.

University of Illinois researcher Elizabeth Jeffery has learned how to maximize the cancer-fighting power of broccoli. It involves heating broccoli just enough to eliminate a sulfur-grabbing protein, but not enough to stop the plant from releasing an important cancer-fighting compound called sulforaphane. The discovery of this sulfur-grabbing protein in the Jeffery lab makes it possible to maximize the amount of the anticarcinogen sulforaphane in broccoli.

Ergothioneine is a naturally-occurring amino acid and is a thiourea derivative of histidine, containing a sulfur atom in the imidazole ring. This compound is made in rather few organisms, notably Actinobacteria and filamentous fungi.[1] Ergothioneine was discovered in 1909 and named after the ergot fungus from which it was first purified, with its structure being determined later, in 1911.[2] This amino acid has antioxidant properties, but its chemistry differs from conventional sulfur-containing antioxidants such as glutathione or lipoic acid. Although ergothioneine cannot be made in human cells, it is present in some tissues at high levels as it is absorbed from the diet.[3] In humans ergothioneine is taken up from the gut and concentrated in the tissues by a specific transporter called the novel organic cation transporter. However, even today, one hundred years after its discovery, precisely what ergothioneine does in the human body remains a mystery

Did you know that cutting the florets into smaller pieces and the stems into thin slices and letting them sit for 5 to 6 minutes before cooking will enhance their cancer protective properties? Cutting broccoli into smaller pieces breaks the cells and activates an enzyme called myrosinase. The myrosinase converts some of the sulfur-containing chemicals found in broccoli (call glucosinolates) into other sulfur containing chemicals (called isothiocyanates) which research has shown to contain cancer preventive properties not found in the glucosinolates . Studies have actually pinpointed specific mechanisms, like changes in cellular genetic processes, which are involved in increasing cancer protection.

Scientists have known that cruciferous vegetables contain a host of chemopreventive agents that act in many different ways to block cancer development.2 Key among these products are indole-3-carbinol (I3C) and sulforaphane.1,3 Cancer cells need a brisk blood supply to support their rampant growth and reproduction. Preliminary studies in vitro and in vivo have found that apigenin inhibits blood vessel growth (angiogenesis) in human ovarian cancer cells, blocking production of two main signaling molecules required to stimulate vessel growth.20,21 Scientists confirmed this effect in ovarian cancer cells, also finding that apigenin strongly inhibits cell proliferation.22 Apigenin and BITC: Complementary Cancer Protection Cancer cells also need energy to support their frenetic reproductive activity. Researchers applied apigenin to human pancreatic cancer cells in culture and studied the cells' uptake of glucose.14 Astonishingly, they found that apigenin deprived energy-hungry cancer cells of glucose to support their voracious appetites and aggressive growth. It did this by down-regulating vital glucose-transporting proteins in cancer cells. This approach could effectively starve deadly cancer cells and stop them in their tracks. Another cruciferous vegetable component receiving rave reviews is the sulfur-containing molecule benzyl isothiocyanate, or BITC (pronounced "bitsy"). As with apigenin, population studies have shown that higher intakes of BITC correlate with reduced risk of cancers of the lung, breast, and colon30 while blocking cancer development in a host of different ways. BITC induces breast cancer cell death by apoptosis (programmed cell death), interfering with cancer cells' energy utilization and causing them to die off before they can contribute to tumor growth.31,32 In human ovarian cancer cells, BITC induces apoptosis by a different mechanism. It stimulates "signaling" molecules that tell cancer cells it's time to close up shop.