by Ashley E. Mason on January 3, 2011
A recent study in the British Journal of Nutrition demonstrated the benefits of grass-fed beef over grain-fed beef. Many of us have heard that grass-fed meats are superior to grain-fed meats for a variety of reasons, and demand for grass-fed beef is definitely increasing. Environmentalists tell us that mass-production of corn for the purpose of feeding animals in confined feeding operations (CAFOs) is bad for the topsoil. Moralists tell us that forcing cattle to live in these conditions is inhumane. Nutritionists (well, nutrition scientists, there is a big difference there!) tell us that feeding cattle grain obliterates the fatty-acid composition of the meat such that instead of having an omega 6 / omega 3 ratio of 2 or 3 to 1 (as it would when pastured), the ratio skyrockets. Nutrition researchers report that grain-fed meat is fattier and less nutrient-dense than than grass-fed meat (see citations on the eatwild page for peer-reviewed research, and another study here). To be sure, the grain-fed cattle industry has not wanted this kind of research to come forth, and they’ve even gone so fat as to declare that grass-fed meats contain more trans-fatty acids than grain-fed meats. The grain-fed cattle industry, of course, neglects to mention, however, that conjugated linoleic acid (classified as a trans fat, but it is naturally occurring) is among the most promising anti-carcinogenic compounds that we know of.
Importantly, there is a growing consensus that it is the last weeks of a cow’s life that make the difference in this lipid profile. Specifically, if one feeds a cattle grass all of its life but grain for the last few weeks of its life, the beneficial lipid profile will deteriorate to that of a cattle who was grain fed for its entire life. The opposite also holds: If you feed a cattle grain all of its life and then grass for the last few weeks of its life, the beneficial lipid profile appears. Hence the term, “grass-finished.”
The study? Researchers wanted to know if eating grass-finished animals instead of grain-finished animals would provide a significant increase in omega 3 in the animal meat and if this increase would actually make a difference in blood counts of those consuming the meat. Two groups of Irish people (all with good cholesterol and blood pressure numbers and without any prescription medications) were given weekly portions of beef and lamb, either grass-finished or grain-finished. The animals were “finished” for a minimum of six weeks. Both groups were told to avoid fatty fish and oils rich in omega 3 for the duration of the study. Both groups of people ate roughly 469 grams of red meat a week for four weeks.
Data indicated that grass-finished meat experienced improved plasma and platelet fatty acid composition such that their blood contained less omega-6 and more omega-3. This increase in omega 3 is associated with a more balanced inflammatory response and subsequent better health.
Other important findings: Lipid profiles of the meat-eaters did not significantly differ (HDL, LDL, triglycerides). The serum and platelet fatty acid content was what changed. Those who consumed grass-finished meat experienced higher levels of EPA, DPA, DHA, stearic acid, long-chain omega 3 fatty acids, and total omega 3, along with a reduced omega 6 to omega 3 ratio. Importantly, the omega 6 to omega 3 ratios in our fat cells determine what kind of inflammatory cytokines our platelets will secrete in an inflammatory response, so having too much omega 6 in our platelets results in an unhealthy, overly-inflammatory response.
Of course, at the end of the day, fatty fish still reign king (wild-caught salmon, and other wild fish) with respect to omega 3 content.
Read the study in the British Journal of Nutrition here.
by Ashley E. Mason on September 6, 2010
Although not overtly stated by authors of recent studies on sugar and cancer, links between sugar consumption and cancer proliferation are appearing in the cancer research literature under the guise of pharmaceutical research. Earlier in August I posted about the unique ways in which fructose, but not glucose, contributed to accelerated tumor growth. Research from the Yokohama City University School of Medicine in Japan and the National Cancer Institute in Bethesda recently published their findings concerning the effects of a drug often administered to Type II diabetics, called Metformin, on colon cancer lesions and lung cancer cells, respectively, in the journal Cancer Research Prevention. Metformin was derived from the French lilac plant (Galega officinalis) in France in the 1950s, and entered the US drug market in 1994 as Glucophage, which means “glucose eater.” The drug, later generically released as Metformin, assists in stabilizing blood sugar by limiting the liver’s output of glucose and increasing the use of sugar by muscle tissue. The authors discuss complex protein activation pathways as potential mechanisms of action, but in my view, failed to take a step back and consider the mechanistic process on a more macro level.
Although the authors of these studies did not focus on the previously established findings that Metformin inhibits the formation of Advanced Glycation Endproducts, or AGEs, this is an important avenue to consider. AGEs and reactive oxygen species*, which are both potentially toxic, are formed when we consume and digest sugars. AGEs are produced through a process called glycation, in which a sugar molecule attaches to protein. If blood sugar levels are low, this initial bond can be broken. If blood sugar is high, the process progresses such that these combined AGE molecules bond to each other repeatedly, and sugars continually link proteins together that were never meant to be together (referred to as “cross-linking“). This is problematic, as these proteins (that never should have crossed paths) are now bound together. The A1C test is a direct test of how much glycation is occuring in one’s body, and this measure is generally some 3x higher in Type II Diabetics (who are not receiving treatment).
Understandably, cross-linking introduces cellular changes that were never meant to exist. AGEs have been linked to Type II Diabetes, cardiovascular diseases, Alzheimer’s disease, cancers, neuropathy, and other sensory deficits.
What can we take from this? If metformin inhibits glycation, which decreases the amount of AGEs produced, which in turn leads to fewer incidences of altered gene expression, cross-linking, and other altered cellular properties – all of which are associated with uncontrolled cellular growth (cancer), then perhaps the critical aspect to understand is that metformin inhibits glycation. Hence, it might behoove us to decrease our rates of glycation. How can we do that? One sure way to do this is to decrease dietary carbohydrate (that is, decrease sugar consumption). Of course, the powers that be (Government(s) with research-grant money) would not be huge fans of this interpretation of the data, given the associations between food industries and governments. Perhaps that is why the authors, who would probably like to receive federal/government funding in the future, avoided a straightforward presentation of the logic that follows from their findings.
*Reactive oxygen species are formed when we burn glucose for fuel at the cellular level, and have been associated with a number of diseases, including diabetes. In this process, electrons attach to oxygen atoms, and this renders them able to react with other molecules (they were previously inert). Free radicals are an example of reactive oxygen species. All reactive oxygen species are all called oxidants (hence, lay references to anti-oxidants as being good, as they are thought to neutralize reactive oxygen species).