The Weston A. Price Foundation has a tremendous opportunity to access an independent research laboratory where we can further our mission of restoring nutrient-dense foods to the human diet through research, education, and activism. But we need your help to realize this goal!
The research lab is the Burnsides Research Laboratory at the University of Illinois, Urbana-Champaign, which for many years has been guided by the esteemed Dr. Fred Kummerow. It was Dr. Kummerow who over 40 years ago performed research showing the damaging effects of trans fatty acids, a fact which Americans now take for granted.
Today, at age 98, he continues to do research on the causes of heart disease. Just as we have predicted, Dr. Kummerow has shown a link between oxidized cholesterol, vegetable oils and heart disease. (See this link: http://www.sciencedaily.com/releases/2013/02/130227151254.htm and the text below this letter for more information on Dr. Kummerow’s latest research.)
And Dr. Kummerow’s legacy continues with the work of post-doctorate Chris Masterjohn, PhD. Chris is using the Burnsides Lab to study the interactions between fat-soluble vitamins A, D, and K, examining the protective effects of vitamins A and K on soft tissue calcification otherwise caused by vitamin D consumed in isolation. Chris’s research will provide important insights into the fat-soluble vitamins, the key to healthy traditional diets, as discovered by Dr. Weston Price.
As you can see, the Burnsides Lab plays a key role in maintaining the legacy of Dr. Price as well as the scientific discoveries of tomorrow. Here’s where your help comes in.
We have been assured by the university that $300,000 per year will allow WAPF to have complete access to the laboratory to do our important research. Just imagine the opportunity this presents for us!
- Chris Masterjohn, PhD, can do further research on the fat-soluble vitamins, including the testing of various foods for levels of vitamins A, D, and K.
- We can research harmful additives in our foods, such as hexane.
- We can investigate the impacts of various cooking and preparation techniques on the nutrient profile of the foods we eat.
- And so much more!
This is the opportunity we have dreamed of–to do the research that will answer the questions we have about nutrient-dense traditional diets.
Please donate today to help us meet our goal. We have already raised $100,000, but we are unable to obtain the remaining $200,000 from existing sources. Won’t you help us make up the $200,000 shortage?
We have set up a link to make it easy to donate to the research lab: https://donatenow.networkforgood.org/wapfresearchlab
Thank you for your support of the Weston A. Price Foundation. Helping now to the best of your ability will go a long way in turning this tremendous opportunity into a reality.
We will keep you updated on the progress of this campaign. Thank you in advance for your help.
Sally Fallon Morell, President
The Weston A. Price Foundation
We would be grateful if you would forward this letter to those on your email list, share it on Facebook and blog about it if you have a blog. Go to westonaprice.org/lab to find a link to this letter, a link to the donate page and donate buttons that you can add to your website or blog. We appreciate your using social media to help us achieve our goals!
It’s easy to donate: Just click here to get started.
Science News… from universities, journals, and other research organizations
Lipid Researcher, 98, Reports On the Dietary Causes of Heart Disease
Feb. 27, 2013 — A 98-year-old researcher argues that, contrary to decades of clinical assumptions and advice to patients, dietary cholesterol is good for your heart — unless that cholesterol is unnaturally oxidized (by frying foods in reused oil, eating lots of polyunsaturated fats, or smoking).
The researcher, Fred Kummerow, an emeritus professor of comparative biosciences at the University of Illinois, has spent more than six decades studying the dietary factors that contribute to heart disease. In a new paper in the American Journal of Cardiovascular Disease, he reviews the research on lipid metabolism and heart disease with a focus on the consumption of oxidized cholesterol — in his view a primary contributor to heart disease.
“Oxidized lipids contribute to heart disease both by increasing deposition of calcium on the arterial wall, a major hallmark of atherosclerosis, and by interrupting blood flow, a major contributor to heart attack and sudden death,” Kummerow wrote in the review.
Over his 60-plus-year career, Kummerow has painstakingly collected and analyzed the findings that together reveal the underlying mechanisms linking oxidized cholesterol (and trans fats) to heart disease.
Many of Kummerow’s insights come from his relentless focus on the physical and biochemical changes that occur in the arteries of people with heart disease. For example, he has worked with surgeons to retrieve and examine the arteries of people suffering from heart disease, and has compared his findings with those obtained in animal experiments.
He and his colleagues first reported in 2001 that the arteries of people who had had bypass operations contained elevated levels of sphingomyelin (SFING-oh-my-uh-lin), one of several phospholipids (phosphate-containing lipids) that make up the membranes of all cells. The bypass patients also had significantly more oxidized cholesterols (oxysterols) in their plasma and tissues than people who had not been diagnosed with heart disease.
Human cells incubated with the blood plasma of the cardiac patients also picked up significantly more calcium from the culture medium than cells incubated in the plasma of healthy patients. When the researchers added oxysterols to the healthy plasma, the proportion of sphingomyelin in the cells increased, as did the uptake of calcium.
Earlier research, including studies conducted by medical pioneer Michael DeBakey, noted that the most problematic plaques in patients with heart disease occurred at the branch-points of the arteries of the heart. Kummerow followed up on these reports by looking at the phospholipid content of the arterial walls in pigs and humans. He found (and reported in 1994) that the branch points of the arteries in humans and in swine also had significantly more sphingomyelin than other regions of the same arteries.
For Kummerow, the increase in sphingomyelin was a prime suspect in the blocked and calcified arteries of the cardiac patients. He had already found that the arteries of the newborn human placenta contained only about 10 percent sphingomyelin and 50 percent phosphatidylcholine (FOSS-fuh-tih-dul-COH-lean), another important phospholipid component of cell membranes.
“But when we looked at the arteries of people who had had bypass operations, we found up to 40 percent sphingomyelin and about 27 percent phosphatidylcholine,” Kummerow said. “It took us many more years to discover that when you added large amounts of oxysterols to the cells, then the phosphatidylcholine changed to sphingomyelin.”
Further evidence supported sphingomyelin’s starring role in atherosclerosis. When Kummerow and his colleagues compared the blocked and unblocked arteries of patients needing second bypass operations, they found that the arteries with blockages contained twice as much sphingomyelin as the unblocked arteries. The calcium content of the blocked arteries (6,345 parts per million) was also much higher than that of the unblocked arteries (182 ppm).
Other studies had demonstrated a link between increases in sphingomyelin and the deposit of calcium in the coronary arteries. The mechanism by which this occurred was unclear, however. Kummerow’s team searched the literature and found a 1967 study that showed that in the presence of certain salts (in the blood, for example), lipids like sphingomyelin develop a negative charge. This explains the attraction of the positively charged calcium to the arterial wall when high amounts of sphingomyelin are present, Kummerow said.
“So there was a negative charge on the wall of this artery, and it attracted calcium from the blood until it calcified the whole artery,” he said.
Oxidized fats contribute to heart disease (and sudden death from heart attacks) in an additional way, Kummerow said. He and his collaborators found that when the low-density lipoprotein (LDL, the so-called “bad cholesterol”) is oxidized, it increases the synthesis of a blood-clotting agent, called thromboxane, in the platelets.
If someone eats a diet rich in oxysterols and trans fats and also smokes, he or she is endangering the heart in three distinct ways, Kummerow said. The oxysterols enhance calcification of the arteries and promote the synthesis of a clotting agent. And the trans fats and cigarette smoke interfere with the production of a compound, prostacyclin, which normally keeps the blood fluid.
“And that causes 600,000 deaths in this country each year,” Kummerow said.
Kummerow is the author of “Cholesterol Won’t Kill You, But Trans Fats Could.”