What Does Science Say About the "What The Health" Documentary


A health documentary (What The Health) has been recently released on Netflix and is causing some discussion among viewers. The documentary DOES provide some good points of discussion about the current health care system, the benefits of increasing whole plant foods (vegetables, fruits, whole grains, legumes, etc) in the diet, and viewing nutrition as a primary concern with the rise of health complications as well as a possible treatment. However, there are a few glaringly obscene statements made in the film that deserve some scrutinizing.

**Take note: The director, executive producer, and entire team behind the film are filmmakers and activists, (and happen to be vegan), that have NO formal education in nutrition/dietetics/food science/chemistry/biology/physiology, etc but rather an ability to make an emotional connection with an audience in order to tell, and sell, a story.

Here are just a few of the more profound statements made in the film:

"Processed meats CAUSE cancer...and processed meats have a DIRECT link with cancer"

"Sugar does not lead to diabetes, but meat does"

"Within MINUTES of eating meat, there is damage to the arteries"

"Eating 1 egg a day is the equivalent of smoking 5 cigarettes a day"

"Cholesterol (like from eating an egg yolk) COATS your red blood cells"

"Fish are mercury sponges that can kill you"

"Highest estrogenic and cancer-promoting effects from salmon"

"Institutionalized racism due to the recommended intake of dairy foods when many minorities have lactose intolerance"

"Cheese is essentially coagulated cow pus"

"An average male only needs 56g, even 30-40g protein, per day"

"Eating meat based on your blood type or ancestral origin is like eating meat because you are a Capricorn"

YES, these are ACTUAL statements made in the film. Not to mention the fact that human testimonials included individuals getting off of dozens of medications in 2 WEEKS! (This is not only unrealistic, it's downright dangerous).

**Before we get to analyzing some of these strong statements, let's make it clear: this post is NOT an argument for/against veganism. Veganism can be a totally respectable and healthful lifelong diet (as long as it is nutritionally adequate) and personally, I can agree with the notion that a diet high in whole plant foods would certainly be more beneficial for health than a diet low in whole plant foods. In fact, any diet can be a respectable and healthful lifelong diet as long as you are obtaining appropriate nutrient intake (calories, macronutrients, micronutrients, fiber, water, etc). This is where the arguments can get muddied: oftentimes emotional bias can skew our views of diets that are different from our own. We tend to view the world through our OWN lens, and not seeing/accepting it for what it is. But for the purpose of this post: I want to clarify some of the strongly stated misconceptions that were made so that you are not being led under false pretenses.

First let's look at the claim that "processed and red meats CAUSE cancer or have a DIRECT link to cancer"...(again, YES these are actual statements made in the film)

Scientific evidence will almost NEVER come to the conclusion of causation or a direct link between dietary intake (in this case, meat intake) and cancer in humans because there are too many other confounding variables, and factors associated with chance and bias that weakens the results. (Turner and Lloyd, 2017) [Association does NOT imply causation] These claims of cancer causation (and further labeling of processed and red meat as carcinogenic) are solely based on animal and in vitro studies, NOT human trials. (Turner and Lloyd, 2017) Human observational studies (i.e. NOT controlled, but rather making observations of associations between diet/lifestyle and cancer risk) may show increased risk of colon cancer in those whose diets happen to contain high amounts of meat, as well as physical inactivity and smoking. (Turner and Lloyd, 2017) In this case, the lifestyle habits of high meat intake may come in conjunction with other factors like low fiber intake, low intake of fruits and vegetables, being physically inactive, smoking, etc. There are also study findings to suggest that adiposity and BMI are larger predictors of this association than just meat intake alone. (Chai, et al. 2017) In this study, a positive association was observed with processed and red meat intake and inflammation, but only when BMI and adiposity were not adjusted for. (Chai, et al. 2017) This means that when the results were controlled for BMI (remove any possible influence of BMI), the association observed between meat and inflammation did not exist. (Chai, et al. 2017) This suggests that it is increased BMI and adiposity that mediates this inflammatory response to increased intake of processed and red meat (i.e. being overweight/obese AND eating high amounts of red and processed meat, NOT the meat itself). (Chai, et al. 2017)

The fact that the film links "meat and animal food intake to being the CAUSE of diabetes"...

As stated above, there is hardly ever a claim in scientific literature that a dietary component, like intake of meat and animal foods, is a CAUSE for a condition, like diabetes. Much of the time these claims are based on animal and in vitro studies, or misinterpreted from associations drawn from observational human studies. [Again, association does NOT imply causation.] In this case, some of these observed associations are likely attributed to the entire diet/lifestyle structure that coincides with a high intake of meat and animal foods where it could be argued that if a majority of your food intake comes in the form of animal foods (protein and fat), then you are likely not getting enough high fiber, and nutrient-dense whole plant foods. (Mari-Sanchez, et al. 2016). Recall from previous posts about the importance of nutrient intake from all whole foods (in terms of calories, macronutrients, micronutrients, fiber, water, etc). [You could argue that a diet that is primarily composed of animal foods is also likely to be low in fiber-rich foods.] It would make sense then why nutrient-dense and fiber-rich diets like the Mediterranean diet have been associated with reduced risk and improvements in type 2 diabetes (as there is more dietary balance). (Mari-Sanchez, et al. 2016) A Mediterranean diet emphasizes plant foods like vegetables, fruits, whole grains, legumes, nuts, olive oil and fish with low meat consumption (notice there is still animal protein intake, but it is not the emphasis of the diet) and a high amount of monounsaturated fatty acids (like olives, nuts, avocados, etc) compared to low amounts of saturated fats (from animal foods).**Personally, I would argue that it is the FIBER content of a diet that poses the greatest risk for diabetes where LOW fiber intake can come from both a high intake of animal foods AND/OR a high intake of refined 'free sugars'. In either case, low fiber intake can likely be associated with calories and nutrients coming in, but without the digestive aid to facilitate appropriate TIMING or RATE of digestion (i.e. nutrient utilization and bulk elimination from the body).

Take note however: there is a link associated with processed meat and increased risk for diabetes compared to fresh meat, and this is likely due to other compounds created during the processing of the meats. (Kouvari, et al. 2016) In this case, processed meats like bacon, sausage, deli meats, hot dogs, salami, etc are associated with increased risk for diabetes whereas fresh meats like beef, lamb, pork or game were suggested to not only NOT share this relationship, but to possibly be beneficial in providing nutrients. (Kouvari, et al. 2016) One of the theories behind meat consumption increasing risk of diabetes is based on the effects of AGEs (advanced glycation end-products) where as a result of high heat (grilling or smoking) and/or addition of sugar compounds (like a BBQ sauce, marinade, or use of sugar in curing meats like bacon and ham) leads to the sugar aggregating with proteins (seen as a caramelization or browning effect). These AGEs are associated with increased inflammation and increased HbA1c in diabetics. (Kouvari, et al. 2016) [HbA1c is glycated hemoglobin where, in a diabetic, the glucose in the blood has become stuck on the red blood cell hemoglobin, and stays there for the entire lifespan of the cell (roughly 120 days). HbA1c is therefore a marker for long-term (~3 months) blood glucose concentrations.] This is also where the most cellular damage from diabetes occurs as the glycated hemoglobin are traveling through the blood and getting stuck in small areas like capillaries of the eyes, extremities, kidneys, etc leading to an inability for blood (with oxygen, nutrients, etc) to reach those areas with subsequent cell and tissue damage and a decreased ability to heal from infection.

No, eating meat does not damage your arteries within MINUTES of ingestion.

It actually takes hours to digest food and absorb those broken down compounds in the small intestine before they enter the portal blood (specifically being sent to the liver) to be metabolized and/or further sent through the peripheral blood to their work-specific sites. Note: You do not have a tube that dumps your stomach contents directly into your arteries: any 'particles that are damaging your arteries' were sent from the liver (where they were metabolized or produced). This most notably includes the lipoproteins which are produced by the liver as a package of cholesterol, triglycerides and protein, to be sent to the peripheral tissues. (This is how cholesterol travels in the blood) Take note however: much of the argument posed in this film is based on the idea that the cholesterol, triglycerides and protein that make up lipoproteins are specifically derived from animal products (protein and fat). HOWEVER, triglycerides can be synthesized from both excess fat AND excess carbohydrates, and cholesterol is BOTH synthesized endogenously and derived from dietary intake. (Yes, you do need some cholesterol in the diet as you do not endogenously produce 100% of your requirements).

These lipoproteins can be categorized as:

  • LDL (cholesterol-rich "bad cholesterol")

  • VLDL (triglyceride-rich "bad cholesterol")

  • HDL ("good cholesterol")

When it comes to dietary intake affecting these cholesterol concentrations, it is theorized that an adequate amount of 'healthy' monounsaturated fatty acids can increase HDL ("good cholesterol") concentrations while an adequate amount of carbohydrates can decrease LDL ("bad cholesterol") concentrations. (Song, et al. 2017) According to this study, having too high of a carbohydrate intake was associated with both high triglycerides and low HDL (both are risk factors for CVD) but with an inverse relationship with total cholesterol and LDL (higher carbohydrate intake was associated with lower TC and LDL). (Song, et al. 2017) Conversely, too high of fat intake was also associated with both high total cholesterol and high LDL (both are risk factors for CVD). (Song, et al. 2017) What does this all mean? Too much of either carbohydrates OR fat poses a risk for CVD due to increased LDL cholesterol and/or decreased HDL cholesterol i.e. the overall composition of the whole diet plays the strongest role in CVD/ 'damaging your arteries'

No, cholesterol does not 'coat your red blood cells'.

As noted above, cholesterol travels in the blood via lipoproteins, which again are packages synthesized in the liver and sent to the peripheral tissues, independent of the red blood cells. [ so NO, cholesterol does not simply 'coat' your red blood cells.] There is NO magic tube that dumps the contents of your stomach directly into your blood.

"Eating one egg a day is like smoking 5 cigarettes a day"

This statement comes as a gross misrepresentation of poorly analyzed study results. The original study he is referring to surveyed a sample population (mean age was 62 years old) from vascular prevention clinics where they were asked to recall their dietary habits (number of egg yolks eaten per week X number of years) and smoking history (packs smoked per year) for the past 50 years. (Spence, et al. 2012) YES you read that correct: this study is based on memory (dietary recall of number of egg yolks eaten PER YEAR, and number of cigarette packs smoked PER YEAR) for their LIFE in order to assess lifelong lifestyle habits and their effects on atherosclerosis/plaque formation. (Spence, et al. 2012) Furthermore, alcohol intake and exercise were NOT taken into account (they ONLY compared egg yolks eaten and smoking behaviors with risk for plaque formation). (Spence, et al. 2012) According to this study, those who were in the highest quintiles showed the greatest associations (highest egg yolk consumption of 4 eggs/week and highest smoking behaviors >40 years were associated with greatest amount of plaque formation). (Spence, et al. 2012) HOWEVER these results are based on a poorly designed study method (observations reliant on the memory of dietary patterns for 50 YEARS) and with the statistical analysis that was used (bivariate relationship), this would also imply that the lowest quintile of egg consumption (0-50 eggs per YEAR) was equivalent to the lowest quintile of smoking for 10-20 YEARS. (Olver, et al. 2013) Yes, this study analysis actually proposes that NOT eating eggs is the equivalent to smoking for 10-20 years: this is why you should not always accept a one sentence summary/headline of a study. Additionally, those who fell in the highest quintile for egg consumption were also an average of 13 years older than the rest of the sample, and most importantly, the study left out important lifestyle factors like exercise, average total calories, fat, saturated fat, total cholesterol, alcohol, vitamin intake and use of medications. (Olver, et al. 2013)

"Fish are mercury sponges"

No, fish are not just floating vessels of mercury waiting to kill you. In fact most, if not all, of the fish you will eat in your life (like salmon, cod, pollock, etc) do not contain a high enough level of mercury, nor are eaten in high enough frequencies, to warrant any risk for exposure or toxicity. (Kuras, et al. 2017) In this study, the highest intakes of these fish (800g/week or eating a 4oz serving 7 days/week) still did not increase human mercury concentrations high enough to warrant a risk for toxicity. (Kuras, et al. 2017) This study even proposed that an individual could theoretically eat 14lbs of tilapia, 8lbs of catfish, AND 4.5 lbs of eel WEEKLY and still NOT exhibit mercury concentrations that exceed the upper limit for safety (i.e. NOT even toxicity, just exceeding the SAFE upper limit). (Kuras, et al. 2017) However, higher levels of mercury ARE found in predatory fish like shark, tile fish, king mackerel, swordfish, marlin and tuna to where these fish specifically are recommended to limit or avoid, particularly in pregnancy. (Kuras, et al. 2017) It should be worth noting however: even in these fish species with higher concentrations of mercury, (unless you are at a high risk for complications) you would need to take in high amounts of only these fish in order to reach exposure levels that could warrant a risk. (Kuras, et al. 2017) ** There are interactive guides like this one: http://www.ewg.org/research/ewgs-good-seafood-guide#.WXEAdIjyt1u to see if there are certain fish you may want to limit based on potential risk factors (like if you are pregnant).

And study results suggest that not only is salmon NOT carcinogenic and estrogenic (like it was made to believe in the film), but where the intake of fatty fish like salmon (which are high in the essential Omega-3 fatty acids) showed an inverse relationship with risk of breast cancer i.e. can be preventative. (Kim, et al. 2009)

And what about dairy?

Believe it or not, cheese is NOT 'just coagulated cow pus' but rather a curd formed from the protein and fat of milk that also provides calcium, magnesium, iodine, riboflavin, folate, B vitamins, and vitamins A and E. (Feeney, et al. 2017) [We are talking about real cheese here: not a cheese-like product] This recent study found that total intakes of dairy (including milk, cheese, and yogurt) was inversely associated with body fatness and waist-to hip ratio while total intakes of milk and yogurt was inversely associated with blood pressure and circulating inflammatory markers. (Feeney, et al. 2017) This means that in this study population, those who tended to eat MORE dairy products (both whole and reduced fat) were on average leaner, had lower blood pressure, and showed less inflammation than those who rarely or never ate dairy products. (Feeney, et al. 2017)

And if you're turned off by the term 'pus'...

The word 'pus' is used in the film as a gross-out scare tactic. What it actually alludes to is leukocyte content (white blood cells) which believe it or not, are present in ALL forms of milk: yes, that includes breast milk. This is a way in which infants can gain immune benefits from breast milk (the transfer of leukocytes, as well as immunoglobulins and much more, from the mother to the baby). (Ballard and Morrow, 2013) The reason why there is a limit to the leukocyte content of cow's milk is the presence of HIGH concentrations of white blood cells could imply the presence of an infection or inflammatory stress. Thus, having a limit is a way to monitor safety of the product.

Is having a dairy food group really 'institutionalized racism' ?

In the documentary, a gentleman tried to explain how lactose intolerance is more widely prevalent than is recognized, particularly in minority populations like African Americans. This IS an accurate statement. However he then goes on to say that the addition of a dairy food group on the USDA MyPlate recommendations is a form of 'institutionalized racism' because it is forcing people (like in ethnic populations where lactose intolerance is prevalent) to eat foods that make them sick.

First let's make it clear here: when the USDA food pyramid changed to the MyPlate, the dairy food group was changed to an optional group (it is pictured as a separate glass, NOT as a part of the plate itself) which alludes to a change from a recommended requirement to a recommended OPTION. (As in, YOU have the choice) In fact, for the most part, YOU have a choice in absolutely anything and everything you put in your mouth. The one caveat to this would be in the case of mislabeling or adulterated products (primarily in the case of supplements as these are not regulated and could therefore contain ingredients in the product that are not present on the label). If someone is unable to digest diary (which is actually more prevalent in the population than people may realize), then don't eat it!

The statement that "as an average sized male, you really only need 56g, or even 30-40g protein a day"

This statement is extremely short-sighted. These suggested amounts of protein may be an acceptable lower limit to simply stay alive (like if you were spending a month in the wild on a survival show). However the 'average male' (let's say 185lbs) would need AT THE VERY LEAST 67g protein, according to the current dietary guidelines of 0.8g/kg body weight (but recall from my protein post that this would be a minimum for adequate functioning-not necessarily optimal functioning). When looking at the proposed even lower protein intake of only 30g PROTEIN PER DAY, this may be appropriate for an individual who is AT MOST 82lbs and is NOT undergoing any growth, illness, repair, physical activity, etc. (i.e. even a child or an elderly person who weighs 82lbs would need more than 30g protein per day, let alone an 'average sized male').

Lastly, we can't ignore this gem: 'that eating meat because of your ancestors or blood type is like eating meat because you are a Capricorn." Yes, this individual actually compared the evidence of biological and ancestral lineage with the practice of believing in a zodiac sign.

Guess what...there is continually mounting evidence on the role of ancestral geographic origins having an influence on our genes. While 'eating for you blood type' is not yet definitive, there is evidence to suggest that the occurrence of various genetic mutations (and enzyme deficiencies) can have a link to ancestral geographic location and ethnic groups. (Luzzatto, 2012) For example, it is suggested that sickle cell anemia (a genetic mutation where the red blood cells sickle in shape after delivering oxygen to the tissues) is associated with protection against malaria. (Luzzatto, 2012) The theory proposes that the high rate of sickle cell trait in individuals from regions where malaria is prevalent is linked to a genetic survival adaptation (which means that due to the high risk for malaria in these specific regions, these genetic adaptations took place over generations to prevent the spread of infection). (Luzzatto, 2012) When it comes to nutritional intake, there are theories suggesting enzyme deficiencies (which can affect ability to utilize nutrients based on dietary intake) have some association with ethnicity (and subsequent ancestral geographic origins). In many non-Westernized societies, native diets can be drastically different worldwide based on both food availability and biological adaptations in the humans eating those foods. It is suggested that these biological adaptions arise in order to best utilize the foods they ARE exposed to. **The big takeaway is this: nutrition is not a cut and dry, one-size-fits-all practice but rather a continually complex and growing area of exploration and adaptation. What works for one person may not work for another, but that does not mean that one is 'right' and one is 'wrong'.

Take from this what you will, but never stop learning.

References:

Ballard O, Morrow A. Human Milk Composition: Nutrients and Bioactive Factors. Pediatric Clinics of North America. 2013; 60(1):49-74. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3586783/

Chai W, Morimoto Y, Cooney R, et al. Dietary Red and Processed Meat Intake and Markers of Adiposity and Inflammation: The Multiethnic Cohort Study. Journal of the American College of Nutrition. 2017; 36(5):378-385. http://www.tandfonline.com.proxy.lib.fsu.edu/doi/full/10.1080/07315724.2017.1318317?scroll=top&needAccess=true

Feeney E, O'Sullivan A, Nugent A, et al. Patterns of dairy food intake, body composition and markers of metabolic health in Ireland: results from the National Adult Nutrition Survey. Nutrition and Diabetes. 2017; 7: http://www.nature.com/nutd/journal/v7/n2/full/nutd201654a.html?foxtrotcallback=true

Kim J, Lim S, Shin A, et al. Fatty fish and fish omega-3 fatty acid intakes decrease the breast cancer risk: a case-control study. BMC Cancer. 2009;9: 216. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2711973/

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Kuras R, Janasik B, Stanislawska M, et al. Assessment of Mercury Intake from Fish Meals Based on Intervention Research in the Polish Subpopulation. Biological Trace Element Research. 2017; https://link-springer-com.proxy.lib.fsu.edu/article/10.1007%2Fs12011-017-0939-9

Luzzatto L. Sickle Cell Anemia and Malaria. Mediterranean Journal of Hematology and Infectious Diseases. 2012; 4(1): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3499995/

Mari-Sanchez A, Gea A, Basterra-Gortari F, et al. Meat Consumption and Risk of Developing Type 2 Diabetes in the SUN Project: A Highly Educated Middle-Class Population. PLoS One. 2016; http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0157990

Olver T, Thomas G, Hamilton C, et al. Putting eggs and cigarettes in the same basket; are you yolking? Atherosclerosis. 2013; 227(1):184-185. http://www.sciencedirect.com.proxy.lib.fsu.edu/science/article/pii/S0021915012008726?via%3Dihub

Song S, Song W, Song Y. Dietary carbohydrate and fat intakes are differentially associated with lipid abnormalities in Korean adults. Journal of Clinical Lipidology. 2017; 11(2):338-347. http://www.sciencedirect.com.proxy.lib.fsu.edu/science/article/pii/S1933287417300211?via%3Dihub

Spence J, Jenkins D, Davignon J. Egg yolk consumption and carotid plaque. Atherosclerosis. 2012; 224(2):469-473. http://www.sciencedirect.com.proxy.lib.fsu.edu/science/article/pii/S0021915012005047

Turner N, Lloyd S. Association between red meat consumption and colon cancer: A systematic review of experimental results. Experimental Biology and Medicine. 2017; 242(8):813-839. http://journals.sagepub.com.proxy.lib.fsu.edu/doi/pdf/10.1177/1535370217693117