ARE ANIMAL PRODUCTS HEALTHY TO EAT? E1
TRANSCRIPT & SOURCES
All around the world, animals and their byproducts are eaten in great abundance. Most people are raised on animal products, so they never question their safety and healthfulness. With so many fad diets and conflicting theories, it can be hard to separate fact from fiction. Thankfully, the science is in, but unfortunately, most people have not seen the science for themselves or they don’t know how to interpret it. Are animal products healthy for humans? There’s a simple answer, but it requires some explanation.
Cholesterol and Heart Disease
Let’s begin with some fundamentals.
Animal products represent the only source of dietary cholesterol.
Because of a genetic variability with cholesterol baselines, two people who follow identical diets can score differently on serum cholesterol tests. This is absolutely critical to understand when designing an experiment to study cholesterol as a dietary risk factor, and scientists have known this since 1979.
Only one type of study is appropriate when examining the relationship between cholesterol consumption and coronary heart disease. This type of study is known as a metabolic ward study. Other types of study design are not applicable such as cross-sectional population studies and other types of epidemiological studies such as case-control studies or prospective cohort studies. When used to study cholesterol, these types of studies are often funded by the meat, dairy, and egg industries.
Prospective cohort studies are by design incapable of finding a link between cholesterol consumption and heart disease risk.
It’s as if you are having a foot race with your friend to see who is faster, except your friend gets a 10-yard head start. If you both finish the race at the same time, your friend might insist that he is just as fast as you. However, you know he is actually slower because you covered a greater distance in the same amount of time. The same goes for population groups that consume cholesterol; Studies need to account for the starting place.
How to Spot Junk Science
Yet, still to this day, many researchers set up faulty studies that do not normalize cholesterol baseline levels, like in this 2010 meta-analysis which, unfortunately, many people cite all too often. If you look at the references, it is funded in part by the National Dairy Council and one of the lead researchers, Ronald M. Krauss, receives funding from the meat and dairy industries. This is what we call junk science and it proves the aforementioned conflicts of interest.
This is not the only example of junk science when it comes to cholesterol. For instance, if a study starts with what is called a “sick population,” meaning their cholesterol scores are already sky-high, then even a study that normalizes for baseline variability can still show little or no correlation with heart disease risk. This is because cholesterol has an exponential decrease in absorption at higher levels and will form a parabolic arc when you plot the points on a graph.
Often studies will observe individuals who are starting with alarmingly high cholesterol scores and then proclaim that because there was no significant change in serum levels by consuming more cholesterol, that there must not be any correlation. Again, this is because adding cholesterol to a diet already high in cholesterol will not show any dramatic change in serum levels.
By 1997, a meta-analysis of 395 metabolic ward studies by Clarke et al. concluded that dietary cholesterol has a positive correlation with serum cholesterol and coronary heart disease.
Furthermore, the optimal LDL cholesterol range was reaffirmed in 2004 by O’Keefe and associates. According to their study, the ideal range for low-density lipoprotein is 50-70 mg/dl, showing that there is a correlation between LDL consumption and atherosclerosis and coronary heart disease.
“No major safety concerns have surfaced in studies that lowered LDL to this range of 50 to 70 mg/dl.”
This is backed up by findings from von Birgelen et al. that demonstrate a positive linear relation between LDL and coronary plaque buildup above 75mg/dL. These studies properly adjusted for baseline variability, and what do you know? They conclusively demonstrated the toxicity of cholesterol.
“There is a positive linear relation between LDL cholesterol and annual changes in plaque size, with an LDL value of 75 mg/dL predicting, on average, no plaque progression.”
Additionally, vegetarians put on an omnivorous diet had their cholesterol levels rise by 19%, but after only two weeks back on their original diets their cholesterol scores returned to normal.
In 2006, Cohen and colleagues published a paper on the connection between low plasma-LDL levels and its protection against CHD. The results were shocking and showed that even in populations with a high prevalence of cardiovascular risk factors, LDL was associated with a “substantial” increase in coronary events.
“These data indicate that moderate lifelong reduction in the plasma level of LDL cholesterol is associated with a substantial reduction in the incidence of coronary events, even in populations with a high prevalence of non–lipid-related cardiovascular risk factors.”
In 2012, Ference et al. found that decreased exposure to LDL cholesterol in childhood was associated with “a substantially greater reduction in the risk of CHD.”
“Normal” is Not Optimal
It is worth mentioning that there is a misconception that 75% of victims of heart disease fall within the “normal” range of cholesterol levels. This misconception is largely thanks to a 2009 paper by Sachdeva et al. that characterized the normal levels as anything below 130 mg/dl, which is 2-3 times the optimal range established by O’Keefe and associates in 2004. Admittedly, only 1.4% of the patients in Sachdeva’s study fell within the optimal range.
Cholesterol and Cancer
Until now, we’ve only discussed cholesterol as a risk factor for heart disease. In 2011, Kitahara and colleagues proved that higher total cholesterol scores were associated with several different types of cancers by examining nearly 1.2 million Korean adults for 14 years.
We also have a clearly established link between cholesterol and breast cancer development, as shown in this 2012 study by Danilo and Frank.
“…cholesterol is capable of regulating proliferation, migration, and signaling pathways in breast cancer.”
And in a 2006 paper by Li et al., it was shown that cholesterol-rich lipid rafts feed cancer cells and are associated with cellular death. It also doesn’t help that dietary cholesterol promotes the oxidation of LDL cholesterol.
In 2002, J.C. de la Torre published findings that Alzheimer’s is actually a vascular disorder caused by lack of blood flow to the brain because of dietary cholesterol.
It is crucial to remember that we are not only talking about cholesterol in meat. Remember, dairy, eggs, cheese, and other animal products also contain the cholesterol we are discussing here.
Preventing and Reversing Heart Disease
So, if cholesterol is extremely unhealthy, do we have any research demonstrating the cessation or reversal of disease after individuals cut cholesterol out of their diets? In fact, we do.
Dr. Caldwell Esselstyn has been helping patients reverse coronary heart disease with a whole foods plant-based diet for nearly 30 years. He published the bestselling book Prevent and Reverse Heart Disease which was based on the results of his 20-year nutritional study, the longest study of its kind ever conducted.
He continues his involvement in this research to the present, with his initial results being corroborated with follow-up studies like these from 2007, 2008, and 2014, respectively.
There is much more that I would love to cover here regarding the vast subject of cholesterol, but I have decided to make a separate follow up to this video covering some of the common rebuttals to what we have discussed here.
Saturated Fat and Cancer
Just like cholesterol, saturated fat is predominantly found in animal products, with very few exceptions such as coconut, palm, and peanuts – but not all saturated fats are created equal. The very few exceptions of plant-based saturated fats are still much healthier by comparison because they are medium-chain triglycerides which actually help lower LDL, burn fat, and boost metabolism.
Saturated fat raises large-particle LDL cholesterol. Large buoyant LDL particles increase heart disease risk by 44% and small LDL particles raise heart disease risk by 63% as demonstrated in this 2009 paper by Mora and associates.
Both saturated fat and cholesterol cause oxidative stress which directly feeds cancer cells, as demonstrated by Levy et al.
Compare that with Elkan et al.’s findings that a vegan diet reduces both LDL and oxidized LDL, as shown in their randomized 2008 review, and it is clear that saturated fat has an ugly relationship with LDL cholesterol.
“A gluten-free vegan diet in RA induces changes that are potentially atheroprotective and anti-inflammatory, including decreased LDL and oxLDL levels and raised anti-PC IgM and IgA levels.”
Saturated Fat and Diabetes
In 2009, Tonstad and her team asked the question, “What is the prevalence of type 2 diabetes in people following different types of vegetarian diets compared with that in nonvegetarians?” They examined 22,434 men and 38,469 women. They normalized for social class, level of education, age, gender, sleep cycle, illness, diet, physical activity, demographics, and BMI.
What they found, in their own words, is,
“The 5-unit BMI difference between vegans and nonvegetarians indicates a substantial potential of vegetarianism to protect against obesity. Increased conformity to vegetarian diets protected against risk of type 2 diabetes after lifestyle characteristics and BMI were taken into account. Pesco- and semi-vegetarian diets afforded intermediate protection.”
This is backed up by findings that saturated fats cause obesity and insulin resistance by increasing the levels of circulating non-esterified fatty acids and killing insulin producing beta-cells.
“Western diets rich in saturated fats cause obesity and insulin resistance, and increase levels of circulating NEFAs [non-esterified (‘free’) fatty acids]. In addition, they contribute to beta-cell failure in genetically predisposed individuals.”
“This cellular stress response may thus be a common molecular pathway for the two main causes of Type 2 diabetes, namely insulin resistance and beta-cell loss.”
According to this 2013 paper by Estadella and associates, saturated fat can promote lipotoxicity both directly through inflammatory pathways and indirectly through alterations to bacteria in the gut, and that both of these pathways perpetuate a feedback process which elevates the risk factors for various diseases.
A 2006 study led by Nicholls concluded that saturated fat reduces the anti-inflammatory potential of HDL and impairs arterial endothelial function, and that polyunsaturated fat, such as that found in many plant foods, boost anti-inflammatory activity.
The reason all of this is not common knowledge became abundantly clear in 2016 when a lawsuit alleged that the USDA dietary guidelines were established after heaving lobbying by the American Egg Board.
“According to the committee, a Freedom of Information Act request they filed “revealed a money trail from the American Egg Board to universities where DGAC members were employed and persistent industry pressure to weaken cholesterol limits.”
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