Ketosis - an experiment (high protein breakfast recipe)

Since starting this ketosis experiment, I’ve been a bit unsure about the amount of protein to eat. On the one hand, I was inspired to try this out because of Jimmy Moore’s recent posts about nutritional ketosis. He’s going extremely low carb and keeping his protein pretty low, too. I think he’s doing something like 85% fat. I know I wasn’t going to emulate that, but to simply keep my carbs under 50 grams total per day. My original breakdown had me eating a pretty large whack of fat and not a whole lot of protein. I had some good advice from my friend Jen, who urged me to up that to make sure I’m sparing muscle as I lose fat. I was still holding on to the fear that maybe too much protein would convert to glucose and knock me out of ketosis. The jury is still out on that one and it doesn’t look like it is probably the big deal I thought it was. Also, I just wasn’t naturally gravitating to eating as much protein as I thought anyway.


Still kind of confused, I listened to a podcast about protein (great timing – thanks Jimmy!) The expert on there recommended eating a minimum of 30 g of protein per meal for everybody. He said it didn’t much matter how big you are or what gender because that amount is has more to do with blood volume than body mass, which doesn’t vary that much across people. So interesting and so not what I thought. He did not think that the calculations based on body size were necessary. That minimum was good for all, although people who work out a lot would need more for repair. Listening to him speak, it made a great deal of sense so I’m going to try this. It happens to work well within the macronutrient amounts/percentages I’ve been using as my goals – Carbs: 48g/10%; Fat: 114g/70%; Protein: 95g/20% (this is within the framework of a 1900 calorie max, which I rarely even approach, by the way – it’s been in the 1550-1750 range).

The goals are great, but I’m usually short of this on my protein – a bit at lunch and definitely at breakfast. Dinner usually comes close to or hits the mark of 30 grams at a meal. As a result, I’m going to change things up a bit more, focusing first on breakfast. The first step is to stop with the Bulletproof Coffee in the morning. I’ve been getting a bit of protein in with it, but nowhere near the 30 gram level. I’m going to switch to a protein centered breakfast and build the other components around getting 30 grams in during that meal. I have a feeling that this change alone will put me on the right path. I’m also looking forward to stopping the caffeine again. I’m just not feeling all that great lately and I think it’s the caffeine, as much as I hate to admit it. How many times I need to go down this road in order to learn this lesson I’ll never know. Progress not perfection, I guess! A long holiday weekend is the best time to let it naturally get out of my system when I can sleep in and rest as much as I want.

30 grams of protein during the first meal of the day will be a challenge for me. It is not natural for me to eat that much in the morning, period. But I think it’s worth a try, so I’m going for it. To make sure it happens during the first week, I’m going to make the following recipe that I will make in a casserole pan and cut into six pretty large portions. It’s going to be A LOT of food for me, but we’ll see how it goes. I’ll put the nutrient breakdown below as well so you can see how it fits into the context of my overall eating plan.

Sausage, Egg, and Spinach Bake
Serves 6
Each serving contains: 393 calories, 4g carbs, 29g fat, 30g protein

12oz loose breakfast sausage (US Wellness Meats)
1 onion, coarsely chopped (I used red)
2 cups frozen spinach
18 large eggs
Salt, pepper, seasonings to taste (I used a mixed seasoning from Trader Joe’s plus sea salt)
1 tablespoon butter or ghee


Preheat oven to 350 degrees. Brown up the sausage in a large oven-proof casserole pan on medium heat, breaking up the pieces as you sauté. When cooked through, empty the sausage into a large mixing bowl. Using the same pan, now greased from the sausage, add in the chopped onion. When the onions become translucent, add the frozen spinach and cook, stirring often, until thawed and most of the excess water has evaporated. Empty the contents of the pan once again into the mixing bowl. Let the contents of the bowl cool a bit for 5 minutes or so to prevent the eggs from starting to cook right there in the bowl. Use the cooling time to add the salt and spices of choice to the mixture as well as to add butter or ghee to the casserole pan you used to cook the sausage and veggies, using the residual heat to melt the fat and a pastry brush to coat the sides a bit (or grease a casserole dish, if your pan is too small).

Once cooled, push the contents of the bowl to one side and add the eggs on the other side (this just makes it easier to whisk the eggs). Whisk the eggs until fluffy and then incorporate the rest of the mixture before pouring the whole bowlful back into the casserole pan or into the greased casserole dish. Place the pan/dish in the oven and bake until solid, about 30 minutes. The eggs may puff up a bit, but will go back down when you take it out of the oven. Cut into 6 evenly sized pieces and enjoy your 30 grams of protein for breakfast!

Get Out Of Your Head - The Mindful Way

Researchers are finding out that mindfulness has been shown to increase happiness. Originally a Buddhist term, the word mindfulness  is now becoming as ubiquitous as the word Zen. But what exactly is it? Going to the gym and running on the running machine while watching TV is not being mindful. Going through a Qigong or Kung Fu form while concentrating on the breath and the movement is. I’m not judging the person on the running machine. It’s okay to be mindless every now and again, but if our goal is to be happy then factoring in more sessions of mindfulness and less sessions of mindlessness will help us to achieve this. 

A student came to me the other day and said that she’d been meditating for 20 minutes every morning but she didn’t feel any different. For true transformation to occur, we need to integrate mindfulness into our day to day life. The Zen master, Thich Nhat Hanh, advises us to use a ringing phone or a red traffic light as a tool to remind us to come back to ourselves and breath three times. What are we doing with our time now? Are we happy? If not, why not? Willpower is like the groceries we buy at the supermarket, it runs out. This is why we need to integrate our practice into our daily life so it’s no longer about willpower, it is a habit to us and this habit then becomes a way of life.

For true transformation to occur we need to get out of our heads. What I mean by this is we need to give our mind a break and ground ourselves in our body. Since coming to the UK, I have seen many people on a Friday night going to a pub and drinking lots of beer and wine. My students have told me that they are getting out of their heads. In China we don’t have this culture, so at first I couldn’t understand why people stand up all evening in a crowded room and drink a lot and don’t eat anything. But now I understand. These people feel stress and this is the only way they know to get away from their stress. But their way is mindless rather than mindful and it will only give them temporary relief and a headache in the morning. A Qigong or Kung Fu Workout is a mindful and positive way to deal with stress. 

Our body is a miniature universe and our Qi is the inexhaustible energy of the universe which underpins our existence. It’s always there for us, just as a waterfall is always flowing regardless of whether we are there to look at it or not. Going through a Qigong or Kung Fu form helps us to be mindful. It shifts our energy and focus from our small mind with its endless circle of thoughts, plans and worries to our universal mind. It stimulate brain chemicals in our mind that are linked to happiness. If our mind and body are in harmony then peace naturally occurs without us having to work at it. Tapping into the universal mind gives us a happiness that no one can take away from us. Happiness is our most natural state of being. We deserve it.

Meditation Aids help us to live happily in the present moment. 

Ketosis - an Experiment (treat edition)

You'd think that keeping total carbs below 50 grams would completely nix the idea of treats. But where there's a will, there's a way! For the most part, I do shy away from sugar based as well as artificial sweeteners. But I've come to realize that a little can go a long way and that having a bit of a treat to look forward to does have a positive psychological benefit. I mostly use Stevia to satisfy the sweet taste, but will also sometimes add a very small quantity of maple syrup, honey, or even regular sugar to things to give them a more authentic taste, without adding significant carbs (under 5g per serving does not bother me or spike cravings).

I should also mention that I've decided to stay mostly dairy free (except butter and ghee). As exciting as it was to think about eating cheese and heavy cream again, I realized that I'm better off without it and don't really miss it right now. I still deal with seasonal allergies which is a sign that my gut is still not completely healed. I suspect my inconsistency with dairy may be playing a part.

So far, I've come up with several treats that I've been enjoying all the while staying comfortably in ketosis. The first is this amazing recipe for Caramelized Coconut Chips from Melissa Joulwan. It is incredibly simple, fast, and more delicious than it has any right to be. Seriously, folks. I am addicted. It has the slightly crunchy appeal of popcorn with the additional saving grace of being super filling. I make it by the half cup and that is perfect for satisfying the snack monster without derailing my experiment. Win-win!

Second up is a crustless key lime pie recipe that I made in tiny 4oz jars subbing a dropperful of stevia for the honey. The dominant tart taste from the freshly squeezed key limes really made this turn out great even with only using the stevia.

My next attempt was chocolate mouse. I did use a tablespoon of maple syrup in edition to a few drops of stevia, to give it a more decadent taste. Keeping the portion small kept the amount of actual sugar eaten per sitting quite negligible. I made half the recipe linked above, and split it into 3 little jars. Using the top layer of cream from regular full fat coconut milk really makes this taste rich and the portion size turned out to be just right. I love how real, healthy fat like that in coconut, is so satisfying and self limiting. It's truly impossible for me to eat too much - a few bites and I've had enough. It's amazing! Another plus is that it really did take less than 5 minutes.

Another good one that hits the chocolate spot is the fat bomb. I'm still perfecting this one - I keep forgetting to add a bit of salt since I use unsalted ghee instead of the salted butter called for. I think that will round out the flavor. I am really looking forward to my new chocolate powder, cocoa butter, and vanilla I ordered. I am imagining all sorts of yumminess I can create with those! If I'm going to be this low carb, some quality ingredients DO make a big difference.

Last but not least, I made some homemade jello using Great Lakes Gelatin and brewed herbal tea, sweetened with a little stevia. Since the ingredients are all carb free and almost calorie free no less, I made these in larger jars. I made two each of orange and apple flavored teas. I'm always looking to get more gelatin in for joint health and gut healing, so this is a big win for me.

My first week of intentionally eating a ketogenic diet has been much easier and less stressful then I would have imagined. I think the transition was helped by the fact that I was really only going from a low carb (75-150 grams per day) diet to a very low carb diet (under 50 grams). Not being completely dependent on sugar to begin with made a big difference. However, as small a change as this may seem, I think it's a critical one for me. Keeping carbs at this level has completely evened out and stabilized my appetite as well as gotten rid of the intrusive cravings. Though by no means an "easy" lifestyle, it does feel sustainable for no other reason than it keeps food more in its rightful place instead of dominating my thoughts and life to a large extent as in the past. I am still the foodie I've always been, loving to cook, try new things, and share my creations with others. But I'm starting to feel more focused about it now that I feel like I'm running the show instead of my cravings.

Ketosis - An Experient (update #1)

I’m in to my second day of the Ketosis Experiment and I’m loving it so far! I went in to it shooting for 5% carbs, 20% protein, and a whopping 75% fat. It is fascinating (to my nerdy brain!) to look at how it all shakes out on My Fitness Pal. You’d think that eating 75% fat would mean eating spoonfuls of mayo or something, but it’s not like that at all. Since fat is so much more calorie-dense it doesn’t take much to keep those numbers high. It’s mostly just using it liberally, but not superfluously.


I’ve found that keeping carbs to 5% is really tough, even with limiting things to the regular low carb freebies of veggies, lime juice, etc. As a result, I’ve rebalanced to 10% carbs (48 grams), 15% protein (71 grams), and 75% (158 grams) fat. That ratio keeps me just under the ketosis threshold of 50 total carb grams a day (generally speaking - it can vary), so I think that will work for my purposes. Especially considering some of that total will be fiber, since I’m going off of total carb grams, not “net” carbs (which subtracts out the fiber and sometimes sugar alcohols).

Another surprising thing is that I thought I would have to consciously cut back on the protein, thinking that might be the problem all along. Eating too much can lead to converting some of it to glucose… But no – the last couple of days have landed me at about 15% with just a “normal” amount of it for me. I really thought I was eating much more. I guess a lot of my protein sources come packaged quite nicely with a whack of fat, so that it has less actual protein grams than I thought. Think eggs, bacon, sausage, salami… Or chicken salad made with homemade mayo. But I digress…

Seeing a couple days of info is making me think that the issue is either too many sneaky carbs (I had let many more “treats” into my life lately) or just too many darn calories, although I’m loathe to go THERE. It’s probably a combination of the two. It kind of makes sense, though. When I was heavier, I burned more in general, and now that I’m 45 pounds down, my requirement has gone down. If my intake hasn’t changed, what previously allowed me to slowly lose, is now the amount to maintain. My hope was that I’d naturally adjust via my appetite, but maybe not. But without any data from before, it’s hard to know if my intake has changed at all.

That being said, I’m wary of paying much attention to calories. I do not want to wind up on the disordered train to crazy-town with all this stuff. So, for now, I’m keeping my calorie “goal” the amount the program claims will allow me to lose a half of a pound a week. I’m not putting in any exercise or anything that would offset that number. I’m just leaving it there and alone as a tool that frames the information I’m really after – the macro-nutrient ratios and absolute amounts in grams of each of them. I’m not necessarily going to hit that “goal” every day and I’m trying to ignore it as a ceiling as well. However, I do hate seeing myself go over (a hold-over from previous dieting attempts) so if I need to, I’ll just raise it. I don’t expect that to be an issue, though. I’m probably eating the most that I can expect to over these first few days while I’m getting the last of the excess carbs out of my system and transitioning to a bona-fide fat burning beast. Once that happens, I expect my appetite to naturally go down a bit. But, we’ll see. I feel strongly that I should not feel deprived when making the transition to very low carb. It’s hard enough as it is… I really don’t want to send those “restriction” signals to my brain in any way. That is a sure way to derail this process.

So for now, I’m shooting to keep my intake just shy of my regular needs and I’m not going to worry about exercising for the calorie burning effect. Instead, I’ll keep up with my yoga (2x), high intensity interval training (1x), tai chi (1x), and walking (daily) for the positive psychological and hormonal effects.

I know I’m only a couple of days in to this, but I’m feeling really great about the experiment. Seeing exactly where I’m at nutritionally has been eye-opening already and I can’t wait to see what else I’ll learn, not to mention that I’m hopeful that these changes will lead to getting the fat loss going again.

Forks Over Knives and Healthy Longevity: A Missed Opportunity for the Cholesterol Skeptics

This is the first part of a series of posts that addresses the science regarding plant based diets and the documentary Forks Over Knives and the very serious inaccuracies and omissions that compromise the critiques authored by the cholesterol skeptics, in particular Denise Minger. 

Food Shortages, Cardiovascular Disease and All-Cause Mortality in the World Wars

In Forks Over Knives, Dr. Caldwell Esselstyn described the classical findings from a paper authored by Strom and Jensen, who observed that in Norway between 1938 and 1948 there was a strong relationship between cardiovascular mortality and changes in intake of fat in the form of butter, milk, cheese and eggs, with the changes in mortality lagging behind dietary changes by approximately one year (Fig. 1).1 Denise Minger not only ignored these findings in her critique despite citing the mortality data from the same paper, but instead claimed in regards to a paper on rationing in Norway that animal foods did not decline until after cardiovascular disease mortality had already started declining.2 Minger misleads her readers by confusing the period when rationing was introduced with the period when the intake of animal foods declined. It can be deduced from the data from the Ministry of Supplies cited by Strom and Jensen that rationing was introduced as a result of a declining availability of such products, and therefore introduced after the intake of animal foods had already declined.1

Figure 1. Mortality from circulatory disease, correlated for age; consumption of fat in form of butter, milk, cheese and eggs, Norway 1938-48

Minger also misleads her readers into believing that there was almost an inverse relationship between the changes in animal protein intake and cardiovascular disease mortality in Norway during World War II by inaccurately reporting animal protein intake for the periods of 1936-37 and 1945. In order to verify Minger's interpretation of the statistics (Fig.3), please refer to the table below of macronutrient intake not present in Minger's post (Table 1), as well as the graph illustrating cardiovascular mortality rates (Fig. 2).1 2 In Minger’s own words, 'I pity da fool who doesn’t enlarge this image.'

Table 1. Macronutrient and micronutrient intake for Oslo men from 50 families, 1936-45 

Figure 2. Mortality from circulatory diseases, Norway 1927-48 

Figure 3. Denise Minger’s inaccurate interpretation of the Norwegian statistics 

Minger even posted a 'Fake Correlated Variable' graph, in an apparent attempt to ridicule Dr. Esselstyn, stating that 'For comparison’s sake, this is what a graph would look like if these variables were tightly linked'. Interestingly the 'Fake Correlated Variable' graph was actually remarkably consistent with the actual data (Figs. 4, 5).

Figure 4. Denise Minger’s 'Fake Correlated Variable' graph 

Figure 5. Actual animal protein intake and age-corrected circulatory disease mortality from the cited papers

In Minger’s critique she conveniently omitted the table from this study detailing animal protein intake despite posting the table of intake of individual food groups, and also failed to provide a free link to the paper claiming that she ‘couldn’t find any free copies to link’ despite one being easily locatable by googling the title of the paper, "Food Conditions in Norway during the War, 1939-45". These facts raise very serious questions as to whether Minger's inaccurate report of the data that appears to be heavily biased in favor of an agenda to promote animal foods was in fact intentional.

Minger also claimed that cardiovascular health did not actually improve in Norway during the war years, and that the decrease in cardiovascular mortality was obscured by an increase in mortality from infectious diseases. Minger appears to be either ignorant or unaware that Strom and Jensen provided additional data demonstrating that from over 15,000 operations carried out in Norway that were complicated by danger of thrombosis, the same surgeons found that the occurrence of these complications declined significantly during the period of deprivation of foods rich in animal fats, which then sharply increased after the resumption of intake.3 4 These findings provided strong evidence of actual improved cardiovascular health in Norway during the period of deprivation of animal foods. In Sweden where mortality from infectious diseases actually decreased during the war, there was a record decline in both cardiovascular disease and all-cause mortality during the war years when animal food intake decreased (Fig. 6).2 5 Other researchers also observed a striking decline in advanced atherosclerosis in Finland and Western Germany during the periods of deprivation of animal foods that returned to near pre-war levels after increasing intake.4 6

Figure 6. Percentage of energy from animal foods and mortality from arteriosclerosis and all-causes, Sweden 1940-1944

These observations from the World Wars are unlikely coincidental as they are consistent with the significant decline in serum cholesterol, and mortality from cardiovascular disease and all-causes in former communist nations of Eastern Europe, beginning in the early 1990's when the communist subsidies on meat and animal fats were abolished after the breakup of the Soviet Union (Fig. 7).7 8 Likewise, the significant decline in serum cholesterol, and mortality from cardiovascular disease and all-causes in the pre and early statin period of the second half of the century in developed nations throughout Western Europe, North America and Australasia is partly explained as a result of successful government policies that emphasized dietary changes, particularly a decreased intake of saturated animal fat. One of the best examples is Finland which experienced the most rapid decline of coronary mortality in the world, which was predominantly explained by a significant decline in serum cholesterol as the result of a large reduction in saturated animal fat and an increase in fruit and vegetable intake (Figs. 8, 9).9 10 

Figure 7. Trends in mortality from heart disease in former communist and western nations in men age ≤64

Figure 8. Observed and predicted declines in coronary mortality in males in Eastern Finland 

Figure 9. Observed and predicted decline in serum cholesterol based on dietary changes in Finish men and women without lipid-lowering medication (1, PUFA; 2, dietary cholesterol; 3, SFA; 4, PUFA + dietary cholesterol + SFA; 5, PUFA + dietary cholesterol + SFA + trans fatty acids; 6, observed serum cholesterol)

Randomized controlled trials provide further evidence of a causal association. A meta-analysis of 395 controlled feeding trials established that dietary cholesterol and isocaloric replacement of complex carbohydrates and unsaturated fat by saturated fat raises LDL and total cholesterol.11 In addition a meta-analysis of 108 randomized controlled trials of  various medical and dietary based lipid modifying interventions found that lowering LDL cholesterol significantly decreased the risk of coronary heart disease and all-cause mortality, while modifying HDL or triglycerides provided no clear benefit after controlling for LDL cholesterol.12

Not only does it appear that Denise Minger resorted to distorting the Norwegian data, she was even spineless enough to refer to the number of lives saved from cardiovascular mortality in Norway as being 'nothing to sneeze at' in an apparent attempt to downplay the importance of saving thousands of lives.

Dr. Caldwell Esselstyn and Treating the Cause of CAD

In regards to Dr. Esselstyn’s study of his initial coronary artery disease patients, Denise Minger misleads her readers into believing that 'half' the patients dropped out of the study by confusing the number of patients who had a follow-up angiogram with the number of adherent patients, simply ignoring the 7 patients who adhered to the diet but did not have a follow-up angiogram. There was actually a 75% adherence rate throughout most of this study, and in the more recent and larger decade long study of over 200 patients (known as Treating the Cause of CAD), there was an adherence rate of 91% (Vid. 1).13 14

Minger also suggested that Dr. Esselstyn’s results may have been due to luck as his study was an uncontrolled intervention study. Dr. Esselstyn however did compare the adherent and non-adherent patients. Despite having similar measurable amounts of disease at baseline as the other 18 patients, the 6 non-adherent patients had 13 new cardiac events within the first 12 years of the study despite the fact that they were still receiving standard care. On the other hand, the 18 compliant participants had no further cardiac events while being fully compliant, despite having 49 events during the 8 years prior to the study, of for which most of this time were receiving standard care.13 14 In the newer decade long study of over 200 patients, recurrent cardiac events only occurred in 0.5% of adherent participants, which is approximately 40 fold lower than other dietary or statin based trials (Vid. 1). Minger suggests that these results were due to luck but provided no evidence demonstrating that coronary artery disease can be spontaneously halted or reversed this frequently even when years of medical intervention have failed.

Video 1. TEDxCambridge - Caldwell Esselstyn on making heart attacks history

Dietary Cholesterol, Cardiovascular Disease and All-Cause Mortality

In regards to the information in Forks Over Knives about the disease promoting effects of dietary cholesterol, Denise Minger claimed that one of the reasons the consensus of the medical community that dietary cholesterol raises serum cholesterol and is unhealthy is due to experiments performed on ‘obligate herbivores’, primarily being ‘rabbits’. Minger is ignorant of the fact that literally hundreds of experiments on numerous different omnivorous species, the most relevant being non-human primates have demonstrated that dietary cholesterol has unfavorable effects on serum lipids and induces atherosclerotic lesions.15 Experiments on non-human primates have demonstrated that intake of even small amounts of dietary cholesterol as low as 43µg/kcal, the equivalent found in only half of a small egg in a human diet of 2,000 kcal induces atherosclerotic lesions. Furthermore, there was no evidence of a threshold for dietary cholesterol with respect to an adverse effect on arteries (Figs. 10, 11).16 [Click here for more information regarding study 16]

Figure 10. Subclavian artery from a Rhesus monkey supplementing 43µg/kcal dietary cholesterol. Sudanophilia (black area) is intense in the area of major intimal thickening.

Figure 11. Fermoral artery from a Rhesus monkey supplementing 43µg/kcal dietary cholesterol. Intimal fibrous thickening and disruption of internal elastic membrane differentiate this artery from control vessels of monkeys supplementing 0 dietary cholesterol.   

Minger also failed to mention that several large forward-looking prospective studies on humans found that dietary cholesterol was associated with a significantly increased risk of all-cause mortality, and that it has been consistently shown in studies on diabetic participants that intake of dietary cholesterol and eggs significantly increased the risk of cardiovascular disease and all-cause mortality.17 18 19 20 21 22

Protein Restriction and Healthy Longevity

Denise Minger suggested in regards to the original Indian study cited by Dr. Colin Campbell that in the presence of aflatoxins rats on low protein compared to high protein diets experience an increased risk of premature death. Minger appears to be ignorant in light of the fact that in the majority of studies on rats, especially those that have not been complicated by the administration of large doses carcinogens, protein restriction actually significantly increased maximum lifespan. For example, a review found that in 16 out of 18 studies protein restriction increased average maximum lifespan by approximately 20%, independent of caloric restriction.23 As for carbohydrate intake, increased intake has either been associated with no change or increased longevity.23 The association between protein restriction and longevity has been primarily attributed to methionine restriction, which has shown to increase both mean and maximum lifespan in rodents by on average up to 40%.23 24

Dietary restriction of methionine has also been shown to inhibit and even reverse human tumor growth in animal models and in culture demonstrating that tumors are methionine dependent, yet is relatively well tolerated by normal tissue.25 A review found that the benefit of replacing casein with soy protein on tumor suppression in the animal model was explained in part by the lower quantity of methionine and in part by numerous beneficial plant based compounds.26 For the sake of comparing 'apples and apples' as Minger put it, studies have found that casein is still far more cancer promoting compared to soy protein even when the casein and soy protein diets were formulated to contain equivalent amounts of the 'limiting amino acid' methionine (Fig. 12).26

Figure 12. Total number (A) and total weight (B) of mammory tumors in rats, 25 weeks after N-nitrosomethylurea injection. Diet Groups: Casein, 20% casein; SPI, 19% soy protein isolate; SPI +Met., 19% soy protein isolate formulated to contain the equivalent amount of methionine as the casein group

Compared to whole plant foods, both methionine content and bioavailability is significantly higher in most protein rich animal based foods, with little overlap.24 Therefore protein combining of unrefined plant foods will result in a quality sufficient to support normal tissue, but not the quality found in animal foods that promote cancer and premature death. These rodent studies are consistent with a number of prospective studies on humans that found that diets higher in protein and often fat, primarily of animal origin at the expense of vegetable protein or carbohydrates are associated with an increased risk of all-cause mortality.27 28 29 30

Minger suggested in regards to a study on non-human primates that in the presence of lower amounts of aflatoxins, higher compared to lower intakes of casein do not promote tumor growth. These findings are in disagreement with other studies that administered low amounts of aflatoxin cited by Dr. Campbell that Minger apparently ignored.31 However, the study on non-human primates did not test intermediate levels of protein intake or specific amino acids such as methionine, and Minger failed to cite any studies comparing casein with plant protein, therefore not allowing for a clear interpretation of these results. In studies on non-human primates, compared to casein, soy protein not only leads to genetic changes that are associated with a decreased risk of cancer, but also improvements in body weight, insulin sensitivity, lipid profile, and even decreases atherosclerosis plaques by on average up to 90% (Fig. 13).32 33 34 35

Figure 13. a, Proportion of each group of Cynomolgus monkeys with CAA plaques, defined as intimal thickness greater than half the medial thickness. b, Average lesion size for those monkeys with atherosclerotic plaques. Soy(-), Soy protein with phytoestrogens mostly extracted. Soy(+), Soy protein with phytoestrogens.

A number of randomized controlled trials have demonstrated the damaging effects of animal protein in human cancers. For example, a randomized, placebo-controlled trial found that among men at high risk, those supplementing with milk protein were more than six times likely to develop prostate cancer compared to men supplementing with soy protein.36 Also, a number of tightly controlled feeding trials with human participants have established that heme iron from the protein portion of meat increases the production of NOCs (N-nitroso compounds) in the digestive tract to concentrations similar to that found in cigarette smoke, of which most are cancerous.37 38 Furthermore, a controlled feeding trial found that NOCs arising from heme iron in meat forms DNA adducts in the human digestive tract, and DNA adducts are a well-established marker of cancer.39 These findings are consistent with recent meta-analyses of prospective studies that found that intake of both fresh red meat and heme from meat is associated with a significant increased risk of colorectal cancer.37 40 Based partly on these lines of evidence, in 2011 the expert panel from the World Cancer Research Fund reviewed over 1,000 publications on colorectal cancer and concluded that there is convincing evidence that both fresh and processed red meats are a cause of colorectal cancer.41 Furthermore, a more recent prospective study with over 2.24 million men and women found that compared to participants who consumed less than 1 serving per week, consuming 2 or more servings of meat significantly increased the risk of colorectal cancer.42

The China Study

Denise Minger suggested in regards to the raw data from the China Study that the counties who had the lowest serum cholesterol levels and had the lowest intakes of animal foods had an increased risk of mortality. However, in the China Study animal protein intake was very strongly associated with numerous favorable socioeconomic factors, with household income explaining between 60% and 80% of the variance of intake between counties, likely biasing towards such findings.  Animal food intake was also associated with other favourable socioeconomic factors including access to doctors and hospitals for antenatal consultation and child births, immunisation, avoidance of famine, owning a fridge, a toilet and the ability to read, of which many were associated to some degree with a lower risk of mortality.43 Among the younger population studied in the China Study II, animal food intake was actually a significant predictor of an increased risk, and plant foods of a decreased risk of all-cause mortality despite the fact that the significant inverse relationship between mortality and household income would have biased these results towards the opposite direction (Tables. 2, 3).43 This resembles Dr. Campbell’s observations in the Philippines where the children from the wealthier families that consumed diets rich in animal foods were more likely to develop liver cancer.31

Table 2. Significant predictors of all-cause mortality in the raw data from the China Study II, ages 0-4

Table 3. Significant predictors of all-cause mortality in the raw data from the China Study II, ages 5-14

Forward-looking prospective studies that controlled for socioeconomic factors found that plant based dietary patterns are associated with a decreased risk of all-cause mortality.27 44 45 46 Furthermore, it has been well established from evidence from over 100 randomized controlled trials that lowering LDL cholesterol significantly reduces the risk of all-cause mortality, even in individuals who already have very low baseline LDL cholesterol concentrations similar to that observed in the rural Chinese.12 47 The great majority of the surge in coronary heart disease mortality in Beijing between 1984 and 1999 has been attributed to a significant increase in serum cholesterol explained largely by a 5-fold increase in red meat and egg intake as well as a decline in fruit and vegetable intake. Without improvements in medical interventions the increase in deaths would have been substantially higher.48

Minger also previously claimed that Dr. Campbell’s findings of an relationship between fat, a marker of animal food intake, and an increased risk of breast cancer mortality in the China Study was attributed to the intake of ‘hormone-injected livestock’. She however provided no evidence that consumption of such livestock was widespread in rural China long enough before the mortality data was collected almost four decades ago for this questionable claim to be plausible. However, she did agree that Dr. Campbell’s findings of early menarche as a risk factor for breast cancer as perhaps reflecting a causal relationship ‘given what we know about hormone exposure and breast cancer’. Not surprisingly she failed to mention that animal protein was associated with elevated circulating estrogen in the China Study, and has been associated with a higher risk of early menarche in numerous studies including a cohort of girls born during the 1930s and 1940s, before the widespread consumption of ‘hormone-injected livestock’.31 49 50 51

In addition, Minger previously criticized a number of Dr. Campbell's statements that he made apparently in regards to both the China Study I & II, yet she cited data only from the China Study I.52 With the addition of the data from the China Study II, the relationship between animal foods and an increased risk of breast cancer mortality became significantly stronger, as did plant foods with a decreased risk (Table 4).43

Table 4. Significant predictors of female breast cancer mortality in the raw data from the China Study II, ages 35-69

Furthermore, consistent with the findings from the China Study, the expert panel from the World Cancer Research Fund concluded in 2011 that there is convincing evidence that dietary fiber protects against colorectal cancer, clearly refuting Minger's claims that research on dietary fiber 'outside' of the China Study does not support Dr. Campbell's findings.41 52

Many of Dr. Campbell’s findings in regards to plant based diets and the risk of chronic diseases in China are consistent with much earlier studies from China and around the world. For example, Williams reviewed the medical literature and documentations on cancer from around the world in 1908 long before the widespread use of intensive farming practices, finding strong evidence of an association between plant based dietary patterns and exceptional longevity and very low rates of cancer. Williams also documented that compared to the less affluent parts of Asia that subsisted on plant based diets, cancer was relatively common in the affluent parts of China that could afford animal foods on a frequent basis. He asserted that:53

…cancer is comparatively uncommon in those parts of China where the bulk of the people live on an almost exclusively vegetarian diet, being too poor to purchase any of the various flesh foods which are there used for culinary purposes.

Consistent with Williams's findings on cancer, Snapper found a similar phenomenon for vascular disease. He asserted that:54

In 1940, I confirmed De Langen’s results... by the observation that in North China, coronary disease, cholesterol [gall]stones and thrombosis were practically nonexistent among the poorer classes. They lived on a cereal-vegetable diet consisting of bread baked from yellow corn, millet, soybean flour and vegetables sautéed in peanut and sesame oil. Since cholesterol is present only in animal food, their serum cholesterol content was often in the range of 100 mg. per cent. These findings paralleled the observation of De Langen that coronary artery disease was frequent among Chinese who had emigrated to the Dutch East Indies and followed the high fat diet of the European colonists.

Overall Impressions of Forks Over Knives

Overall, Forks Over Knives provides a lot of very useful information to help viewers make life saving and longevity promoting dietary changes, and best of all comes directly from the doctors who have actually reversed many of the chronic diseases which are leading causes of disability and death. Ignoring the preponderance of evidence favoring a predominately plant based diet, low in saturated fat that is recommended by virtually every respected healthy authority around the world, and instead blindly following the unfounded dietary advice of the cholesterol skeptics can result in absurd consequences and a missed opportunity for healthy longevity.55


Part II: Forks Over Knives and Health Longevity: Perhaps the Science is Legit After All

Please post any comments in the Discussion Thread.

Forks Over Knives and Healthy Longevity: Perhaps the Science is Legit After All

This is the second part of a series of posts that addresses the science regarding plant based diets and the documentary Forks Over Knives and the very serious inaccuracies and omissions that compromise the critiques authored by the cholesterol skeptics, in particular Denise Minger.

Part I: Forks Over Knives: A Missed Opportunity for the Cholesterol Skeptics

Denying the Preponderance of Evidence

Large systematic reviews of the nutritional literature authored by major international health authorities and by panels of leading nutrition researchers, many of which have disclosed ties to livestock industry, have consistently come to the conclusion that diets should be predominately plant based.1 2 3 4 The documentary Forks Over Knives features a number of doctors who have come to the conclusion that the allowance of animal foods in 'small-to-modest' amounts (made by researchers who often have financial ties to the livestock industry) are too permissive and that an optimal diet should be almost entirely composed of minimally refined plant foods. They also conclude that many major chronic and degenerative diseases that affluent populations succumb to can be prevented, and in many cases even reversed by consuming a whole-foods plant based diet. For the vast majority of nutritional researchers the question is no longer as to whether a plant based diet or an animal based diet is more optimal, but as to what the upper tolerable intake is in an optimal diet for foods not derived from minimally refined plant foods.

Many leading nutritional researchers and prominent health authorities actually do agree that the medical literature supports many of the dietary recommendations made by the doctors in Forks Over Knives, but are often unable to make similar recommendations to the public, in part due to socioeconomic factors. For example, Eric Rimm from the Department of Nutrition, Harvard said to Reuters in regards to a major health report produced by the National Academy of Science, which he was an author of that:

We can’t tell people to stop eating all meat and all dairy produces. Well, we could tell people to become vegetarians... If we were truly basing this on science we would, but it is a bit extreme.

Similarly, Walter Willett, the Chair of the Department of Nutrition, Harvard previously said in regards to findings on cancer that:

If you step back and look at the data, the optimum amount of red meat you eat should be zero.

Diethelm et al. published an excellent review addressing the five characteristics of denialism. The first characteristic describes how the cholesterol skeptics attempt to downplay the scientific consensus regarding the disease promoting effects of elevated LDL cholesterol and animal based diets rich in saturated fat:

The first is the identification of conspiracies. When the overwhelming body of scientific opinion believes that something is true, it is argued that this is not because those scientists have independently studied the evidence and reached the same conclusion. It is because they have engaged in a complex and secretive conspiracy.

The cholesterol skeptics will also attempt to downplay the scientific consensus often by insisting that scientists are ignoring certain studies, studies which these denialists fail to mention are compromised by a number of very serious flaws and omissions.5 6 7 Diethelm et al. also explains the motivations behind denialism:

Denialists are driven by a range of motivations. For some it is greed, lured by the corporate largesse of the oil and tobacco industries. For others it is ideology or faith, causing them to reject anything incompatible with their fundamental beliefs. Finally there is eccentricity and idiosyncrasy, sometimes encouraged by the celebrity status conferred on the maverick by the media.

Perhaps the cholesterol skeptics persistent denialism can be explained by conflicts of interest associated with the sales of merchandise or the desire for celebrity status on the internet. Brownell et al. reminds us how serious and real conflicts of interest are, describing the tactics used by the tobacco industry, who for decades attempted to dismiss the 'junk' science linking smoking to lung cancer and other associated diseases, whose personal gain from this caused millions of people to perish. They asserted:8

A striking event occurred in 1994 when the CEOs of every major tobacco company in America stood before Congress and, under oath, denied believing that smoking caused lung cancer and that nicotine was addictive, despite countless studies (some by their own scientists) showing the opposite.

This merits exploration as to whether the cholesterol skeptics motivations are any different than these other denialists, and whether many of the hundreds of peer-reviewed papers they also dismiss as 'junk' science are actually informative and contain potentially life-saving findings.

Hormone Free, Pasteurised Animal Foods and Primitive Populations

Cholesterol skeptics will often claim that the results of any study suggesting harmful effects of animal foods were obscured due to participants consuming unnatural foods produced by intensive farming practices. The cholesterol skeptics however provide scant evidence regarding the perpetrated health benefits of replacing whole plant foods with naturally produced animal foods. Studies cited throughout both Part I of this review and this current post demonstrate that the association between replacing minimally refined plant foods with animal foods and poorer health expectancy can largely be explained by the fact that animal foods are typically naturally rich in methionine, dietary heme, saturated fat, dietary cholesterol, ruminant trans-fat, and hormones, and deficient in dietary fiber, antioxidants, carotnoids and phytochemicals, just to name a few.

A number of studies that have actually found some of the strongest associations between animal food intake and an increased risk of chronic diseases were actually carried out in populations where livestock is primarily grass fed and administration of hormones to livestock are banned by law, such as in Uruguay.9 10 11 12 These studies cannot simply be explained as exceptions as they are consistent with evidence from before the widespread use of intensive farming practices that produce unnaturally raised livestock.

In 1892 the renowned French geographer, Reclus noted that:13

...cancer is most frequent among those branches of the human race where carnivorous habits prevail.

In 1908, Williams published an extensive review of the medical literature and documentation from a large number of populations around the world in regards to the causation of cancer, and came to conclusions that were consistent with Reclus's findings:14

Careful study of the life-history of centenarians and of persons of advanced age who, as we have seen, are very rarely the victims of cancer shows that they are generally of spare figure, medium height, and that they eat frugally, taking but little meat and alcohol....In this connexion, it may be well to recall the fact, that although cancer is remarkably rare in vegetarian communities, yet complete exemption cannot be claimed for such ; and the like is true of herbivorous, as compared with carnivorous animals. In spite of these facts, which indeed are only such as might have been expected from the essential nature of the problem, there cannot be the slightest doubt in face of the overwhelming evidence I have adduced in the course of this work that the incidence of cancer is largely conditioned by nutrition.

In 1925, Kuczynski described the poor health of a population who subsisted on a diet based predominantly on organic pasteurized animal foods. As later described by Stamler:15

Kuczynski (1925) reported on an Asian population at the opposite end of the dietary spectrum - nomadic Kirghiz plainsmen who habitually consumed large amounts of meat and milk. He noted high incidence of obesity, premature extensive atherosclerosis, contracted kidney, apoplexy, and arcus senilis. Their urbanized kinsmen, subsisting on more varied fare, did not exhibit such severe vascular disease.

In 1932, Raab noted in regards to the distribution of atherosclerosis, that:

…the relative rarity of atherosclerosis and hypertension among the chiefly vegetable-consuming inhabitants of China, Africa, Dutch East India, and the enormous frequency of arteriosclerosis and hypertension among the peoples of Europe and North America who consume large quantities of eggs, butter...

In 1934, Rosenthal reviewed 28 papers from observations carried out around the world, and reached a conclusion that was consistent with Raab’s findings, noting that:16

…in no race for which a high cholesterol intake (in the form of eggs, butter and milk) and fat intake are recorded is atherosclerosis absent...

In 1940, based on years of clinical practice and reviewing medical reports, Bertelsen who is considered the father of Greenland epidemiology stated in regards to the mortality patterns amongst the Greenland Inuit that:17 

...arteriosclerosis and degeneration of the myocardium are quite common conditions among the Inuit, in particular considering the low mean age of the population. 

In 1904, Bertelsen proved the existence of cancer in the native Inuit, diagnosing a case of breast cancer. During the following decades researchers documented that the existence of cancer was exceedingly common among the Inuit despite their relatively short life expectancy.18　Consistent with Bertelsen’s findings, an Inuit predating western contact who was mummified in approximately 1475, 450km north of the Arctic Circle was shown to have evidence of cancer, likely of the breast.19 It has also been documented that numerous preserved pre-contact Inuit who were mummified dating all the way back to 1,500 years ago had a severe degree of atherosclerosis, osteoporosis, and osteoarthritis, consistent with studies of Inuit living in the 20th century.20 21 22 23 Other evidence of poor health among the pre-contact Inuit includes iron deficiency anemia, trauma, infection, dental pathology, and children with downs syndrome and Perthes disease.24 25

A large number of the examined mummies from ancient Egypt have also provided clear evidence of atherosclerosis in ancient civilizations. Unfortunately some researchers have previously confused the diets of the mummified elites of ancient Egypt who exhibited atherosclerosis with the plant based diets of the lower classes of Egypt.26 More recent research on the interpretations of the ancient Egyptian hieroglyphs and isotope analysis of hair samples from the mummies has provided strong evidence that the elites of Egypt, being those primarily mummified consumed a diet rich in meat and saturated animal fat.27 28 29 The researchers asserted that:

It is important to point out that there was a marked difference between the mainly vegetarian diet most Egyptians ate and that of royalty and priests and their family members whose daily intake would have included these high levels of saturated fat. Mummification was practised by the elite groups in society, ensuring that their remains have survived to provide clear indications of atherosclerosis; by contrast, there is a lack of evidence that the condition existed among the less well-preserved remains of the [mainly vegetarian] lower classes.

The following videos (Videos 1-6) are from the very inspirational Primitive Nutrition Series produced by Plant Positive, providing further details that address the very serious flaws and omissions that compromise the claims from advocates of animal based diets regarding primitive population studies.

Video 1. Primitive Nutrition 27: The Eskimo Model, Part I

Video 2. Primitive Nutrition 28: The Eskimo Model, Part II

Video 3. Primitive Nutrition 29: The Masai Model, Part I

Video 4. Primitive Nutrition 30: The Masai Model, Part II

Video 5. Primitive Nutrition 31: The Native Australian Model

Video 6. Primitive Nutrition 32: Ancient and out of Fashion

Taking Unfounded Wheat Claims with a Grain of Salt

At least eight large prospective studies consisting of a total of over 1,125,000 participants found that intake of foods containing whole grains or grain fiber were associated with a significantly lower risk of all-cause mortality, even in studies where the primary consumed grain was wheat or other gluten containing grains.30 31 32 33 34 35 36 37 38 These results are very impressive in light of the fact that the definition of whole grains in these studies were typically considered as foods containing as little as 25% whole grain, and that grain fiber intake in most developed nations is largely derived from refined grains, potentially underestimating the benefits of actual whole grain intake.39

A meta-analysis of 7 prospective studies found that intake of foods containing whole grain was associated with a 21% decrease of cardiovascular disease, and a pooled analysis of 11 prospective studies that used dietary validation methods found a 10 g/d increment of grain fiber was associated with a 25% decrease risk of death from coronary heart disease.40 41 Meta-analyses and systematic reviews have also found that foods containing whole grain and grain fiber significantly decreases the risk of colorectal cancer, type II diabetes, hypertension, and obesity.42 43 44 45 Furthermore, multiple studies have found that replacing animal foods with whole grains significantly decreases the risk of type II diabetes.46 47

Denise Minger has been criticised for failing to carry out multivariate analyses in order to adjust for multiple confounding variables simultaneously in her critiques of the China Study. A Swedish blogger carried out a multivariate analyses with multiple response variables from the raw China Study data, finding contrasting results to that of Minger s, primarily that animal protein and fat were associated with an increased risk of ischemic heart disease, whereas green vegetables, dietary fiber and grains, including wheat were associated with a decreased risk (Fig. 1). (48 49 50 English version from Google Translate)  These findings certainly raise questions as to whether Minger's oversimplified analysis holds up to her claims that 'wheat is murder'. When compared to Minger’s analyses, these findings are far more consistent with the findings from major cross-country studies, with the exception of vegetable fat (from PUFA and MUFA), which is typically associated with a decreased risk after controlling for saturated fat.51 52 53 54 These findings are also consistent with the observation that the large majority of the world’s population were largely free from coronary heart disease while consuming their traditional diet centered on tubers, legumes, and grains including wheat prior to adopting a western dietary pattern.55 56 57

Figure 1. Various foods and nutrients and risk of ischaemic heart disease in a multivariate regression analysis with multiple response variables for ages 35-69 in China Study II

Often overlooked by the promoters of wheat free diets is that well fermented wheat eliminates the great majority of gluten and has shown to be tolerable by celiac patients.58 Furthermore both epidemiological studies and randomized controlled trials have found that whole grain wheat does not  promote weight gain or impair satiety and is likely beneficial.59 60 61 62 63 Lastly, the fact that many of the authors of some of the most popular weight loss diet books that advocate the restriction of wheat and grain intake in favor of animal foods have remained over-weight despite apparently following their advocated diets for decades raises further questions as to whether such diets are the most optimal for weight loss and healthy longevity (Video 7). 

Refer here for a very informative review that documents the very serious inaccuracies, omissions, and oversimplifications presented in the book Wheat Belly.

Video 7. Low Carb vs. Plant-Based

Lowering Serum Cholesterol on a Plant Based Diet

Evidence from over 100 randomized controlled trials, large meta-analyses of mendelian randomization studies, and prospective studies consisting of several million individuals have firmly established a causal relationship between lowering LDL and non-HDL cholesterol and a decreased risk of cardiovascular disease and all-causes mortality, without evidence of a threshold beyond which a lower concentration does not provide additional benefit.64 65 66 67 68 69 70 71 

Regardless of the overwhelming evidence, Denise Minger suggested that the cholesterol levels among Dr. Esselstyn’s patients (serum cholesterol, >100mg/dl; LDL, >48mg/dl) are unhealthy and 'super-low'. It has already been established for decades that these 'super-low' cholesterol levels are actually well above levels required in order to support normal growth and development, and are the typical levels that were likely maintained for tens of millions of years throughout human evolution.72 73 These are also the typical concentrations found in free-ranging non-human primates, and among these primates consuming only food founds in their natural habitat higher cholesterol concentrations have been associated with atherosclerosis despite having cholesterol concentrations that Minger may define as 'super-low'.74 These lines of evidence refute the claims suggesting that foods found in nature promote optimal health regardless of their effect on LDL and serum cholesterol. Furthermore, individuals born with extremely rare conditions that cause life-long LDL levels of <15 mg/dl display normal growth and actually experience increased longevity.75 Michael S. Brown and Joseph L. Goldstein who were awarded a Nobel Prize for their research on the metabolism of LDL cholesterol elaborated on in this topic in their Nobel Prize lecture:76

In view of the 10 to 1 gradient between concentrations of LDL in plasma and interstitial fluid, a level of LDL-cholesterol in plasma of 25 mg/dl would be sufficient to nourish body cells with cholesterol. This is roughly one-fifth of the level usually seen in Western societies.  Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl. In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels. Second, the LDL level in newborn humans is approximately 30 mg/dl, well within the range that seems to be appropriate for receptor binding. Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl. It only reaches levels above 100 mg/dl in individuals who consume a diet rich in saturated animal fats and cholesterol that is customarily ingested in Western societies.

Minger made an unreferenced suggestion that Dr. Esselstyn’s patients while having no additional coronary events over several decades while adhering to the prescribed diet, may have somehow achieved better results if they consumed a diet that raised their HDL and lowered their triglycerides. She also made an unreferenced suggestion, perhaps referring to epidemiological studies that lowering cholesterol can increase the risk of developing a number of diseases, including cancer and neurological disorders. As is typical with the cholesterol skeptics, Minger will often dismiss any epidemiological study with findings suggesting adverse health effects of animal based foods as being largely uninformative, insisting that 'correlation isn’t causation'. Therefore this merits exploration into how epidemiological studies compare to randomized controlled trials used to prove 'causation' relating to Minger's concerning comments about serum lipids.

As already mentioned in the first post, a meta-analysis of 108 randomized controlled trials of various medical and dietary based lipid modifying interventions found that lowering LDL cholesterol significantly decreased the risk of coronary heart disease and all-cause mortality, while modifying HDL or triglycerides provided no clear benefit after controlling for LDL cholesterol.77

More recently a meta-analysis of mendelian randomization study of 170,000 participants found that inheriting genetic variants that are associated with life-long elevated HDL do not affect the risk of coronary heart disease.78 Another recent meta-analysis of mendelian randomized study with over 312,000 participants found that inheriting any of the nine studied genetic variants associated with life-long reduced LDL, but do not alter other known risk factors equally predicted a three-fold greater decreased risk of coronary heart disease per unit lower of LDL than statins do when started later in life (Video 8).79 Furthermore, this study and others found that individuals who inherit a variant of the statin drug targeted HMGCR gene that is associated with life-long reduced LDL, have an equal degree lower risk of coronary heart disease as individuals who inherited any of the other 8 studied gene variants.80 81 

These studies provide convincing evidence that the primary mechanism in which statins lower coronary heart disease can be explained by it effects on lowering LDL cholesterol. These studies also provide convincing evidence that the benefit of lowering LDL depends on both the timing and the magnitude of the LDL reduction, and that the benefits associated with lower LDL are largely independent of the mechanism in which LDL is lowered. This in-turn supports the benefits of a plant based diet combined with exercise, the safest way to significantly lower LDL cholesterol, beginning as early in life as possible (Video 8).

Video 8. Long Term Reduction in Low-Density Lipoprotein Cholesterol Beginning Early in Life 

In contrast to prospective epidemiological studies that focused on only base-line HDL, the results from prospective studies that tested the effect of HDL modification and the risk of cardiovascular disease have not been so consistent, for which the largest study failed to find any association after controlling for other risk factors.82

If raising HDL can actually modify cardiovascular risk, then this data provides convincing evidence that it is important to consider the mechanism of HDL rather than the concentration alone. For example it has been shown that diets high in saturated fat impairs the anti-inflammatory properties of HDL compared to polyunsaturated fat, and that high fiber low-fat diets convert HDL from pro to anti-inflammatory HDL.83 84 85 In addition animal fat contains dietary cholesterol and ruminant trans-fat which has been shown to raise the LDL/HDL ratio in randomized controlled trials.86 87 88 Therefore the preponderance of evidence demonstrates that attempting to raise HDL in the presence of an increased saturated animal fat intake as advocated by cholesterol skeptics will only increase the risk of cardiovascular disease.

It is well established that carbohydrate foods stripped of their nutritional value elevate triglycerides, but also that nutrient dense carbohydrate foods do not produce such an elevation, especially when the carbohydrate is largely derived from dietary fiber and resistant starch.89 90 91 92 93 94 This evidence strongly suggests that the elevated levels of triglycerides in a number of Dr. Esselstyn’s participants was a marker of excessive intake of refined carbohydrates that Minger claimed that they had eliminated from their diet. Minger appears to have confused Dr. Esselstyn's recommendations in his recent book with those provided to his initial set of patients well over two decades ago. Dr. Esselstyn did not specify in his papers that his initial set of patients were asked to eliminate refined carbohydrate foods, which may have played a large role in their diets considering that carbohydrate intake was increased to approx. 80% of total energy. The success seen among Dr. Esselstyn's initial set of patients therefore can probably not be explained by a reduced intake of nutrient poor carbohydrate foods.95

In regards to the cholesterol skeptic's typical claims about low serum cholesterol and an excess risk of cancer, an editorial authored by the American Cancer Society attributed this association to reverse causation, refuting the suggestion of a causal relationship:96

Many epidemiologic studies published in the 1980s documented an association between low circulating cholesterol and higher overall cancer incidence and mortality. This association has been attributed to reverse causation, that is, undiagnosed cancer causing a reduction in cholesterol levels. Reverse causation is strongly supported by observations that cholesterol levels decline before cancer diagnosis and that associations between low cholesterol and cancer incidence and mortality weaken when the first few years of study follow-up are excluded. In addition, a meta-analysis of randomized trials of cholesterol-lowering statins found no effect on risk of cancer, although only short-term effects could be addressed due to the short duration of most trials.

More recently several mendelian randomization studies have demonstrated that individuals who inherit genetic variants associated with life-long reduced LDL do not have an excess risk of cancer, compensating for the relatively short-term cholesterol-lowering trials.97 98 99

Minger’s own words, 'Yikes! Did we slip and fall back into the ’80s?' more accurately describes her own misleading statements than that of the doctors in Forks Over Knives. Several recent prospective studies with up to 37 and 40 years follow-up, sufficient to potentially eliminate the possibility of reverse causation found that elevated serum cholesterol was associated with an increased risk of aggressive prostate cancer or prostate cancer death.100 101

In regards to low cholesterol and neurological disorders, a mendelian randomization study found that individuals who inherit genetic variants associated with life-long reduced LDL do not have increased depressive symptoms.102 Also, randomized controlled trials have found that vegetarian diets which are associated with lower cholesterol are also associated with improved moods compared to omnivorous diets.103 104 105 Other randomized controlled trials found that psychological symptoms including depression, hostility and anger improved significantly on a cholesterol lowering, complex-carbohydrate rich diet compared to baseline or carbohydrate restricted diets.106 107 Conversely, systematic reviews and meta-analyses of epidemiologic studies have found an association between dairy intake and an increased risk of Parkinson’s disease, and saturated fat and an increased risk of dementia.108 109 110 111

For the evidence regarding diet and serum lipids and the risk of stroke please refer to Part I and Part II of my review addressing this subject.

The World Wars Revisited

During the British blockade in World War I, the food imports that Denmark heavily relied upon were cut off and the population was forced to sell a large portion of their livestock due to the inefficient conversion of livestock feed into meat. Following a transition towards more of a plant based diet the Danish capital experienced a significant decrease in mortality from chronic disease and all-causes during the period of significant regulation towards the end of the war.112 113

As previously discussed in Part I of this review, in World War II a number of Scandinavian and Low Countries of Europe experienced deprivations of animal foods together with a significant decline in cardiovascular mortality. In contrast, in the United States heart disease mortality increased together with an increased intake of dairy and eggs. In regards to the scarcity of war time tobacco as a potential confounding variable, smoking was very rare among Scandinavian women prior to the war yet cardiovascular mortality decreased similarly in both men and women. Furthermore in nations such as Denmark and Great Britain where there was a similar scarcity of tobacco as other Scandinavian countries but intake of cholesterol rich food was not significantly altered, there was no significant change in cardiovascular mortality. It was also observed that the decline of cardiovascular mortality was in the order of the nations that experienced shortages of animal fats earlier in the war.114 115 116 Another valuable finding was the observation that children born in Norway and other parts of Scandinavia during or shortly after the war experienced lower than expected rates of a number of cancers during the following decades, suggesting the importance of a plant based maternal diet.117 118

During the food shortages in West Germany under the Allied occupation from 1945-48 there was an observed absence of advanced forms of atherosclerosis, diabetic complications and cardiovascular mortality compared to the pre and post occupation period, as well as compared with the parts of Southern Germany that did not experience severe food shortages. This was attributed primarily to a cholesterol lowering diet that was low in energy, animal fat and animal protein and rich in foods high in dietary fiber. Other major modifiable risk factors were unable to explain the changes in cardiovascular disease as these were modified only slightly between 1948-50 when the sharp increase in heart attacks was observed.119  

In regards to dietary intake of Norway during the war, Minger cited evidence from a chart of food intake of men from 50 families in Oslo which included foods obtained outside of rationing from illegal sources. As the authors pointed out, these illegally obtained foods were 'mostly of bread and flour', suggesting that the data for animal food intake cited by Strom and Jensen in Part I of this review was not compromised by the exclusion of illegally obtained foods. Nevertheless, Minger referred to the almost two fold increase of flour, meal and groats during the war as being only a 'slight' increase. The chart suggests that among these men, compared to the 1936-37 pre-war period, intake of meat, eggs and added fats had significantly decreased by at least early 1941 and declined throughout the year. This provides further evidence that refutes Minger s claims that intake of animal foods did not decline until late 1941. However, compared to 1936-37 total dairy intake among these men was observed to be slightly higher in 1941 but then declined from early 1942, primarily from high fat sources.120

Table 1. Dietary intake of food groups for Oslo men from 50 families, 1936-45

In regards to dairy intake in Norway, Denise Minger claimed that:

There’s no doubt about it: In 1941, when cardiovascular disease started plummeting, Norwegians were eating more total dairy (light blue line) than they were before the war, when the death rate was higher. 

Minger derived this data from these same Oslo men from 30 to 50 families (Table 1) and graphed the intake of dairy intake using the per-war years of 1936-37 and the war years of 1941-45. Regarding the dietary intake of these Oslo men Minger clearly contradicted herself by first stating that 'it’s hard to say how accurately this represents the food intake of Norway’s whole population', and then stating 'There’s no doubt about it', as if she is certain that this data accurately reflected the intake of the entire Norwegian population. When examining the observed dietary changes of these Oslo men and cardiovascular disease statistics, it may be more informative to provide statistics specifically for Oslo men, rather than the entire nation as Minger has done, as the observed rates of cardiovascular mortality were significantly different between Oslo men and Oslo women, as well as between Oslo and the entire nation.121 122

In Oslo the observed heart attack rate of men was actually slightly higher in 1941 compared to 1936-37, but then plummeted in 1942 simultaneously with the decreased intake of dairy, particularly from high fat sources. The observed increased heart attack rate in Oslo men in 1945 with an increased intake of diary in early to mid-1945 among these Oslo men (Figs. 2, 3).

Figure 2. Analysis of hospitalized cases of myocardial infarction (heart attack) in a sub-group that was estimated to much more accurately reflect that of the general population in Oslo, Norway 1935-49

Figure 3. Dairy intake and myocardial infarction in Oslo men, 1936-45

Although Minger correctly points out that Dr. Esselstyn did not mention the significant increased intake of fish in Norway during the war years, her claim that the Norwegian diet was 'marine based' appears somewhat fishy. According to the tables of food intake for the Oslo men that Minger focused on, intake of the major starch groups, including flour, meal and groats, bread, potatoes, and roots and vegetables was approximately 1 kg/day, roughly 4 times that of fish intake. Fish intake can not explain the large decline of cardiovascular morality in Scandinavia and the low countries of Europe. In Finland where the observed decline in arteriosclerosis mortality was even greater than in Norway, availability of fish was actually lower throughout most of the period where wartime rates of mortality were plummeting, and also declined throughout the late 1980s and 1990s when mortality was again plummeting.123 124 125 126

Several recent meta-analyses of randomized controlled trials, including the highest quality double-blinded, placebo-controlled trials failed to show that fish oil decreased the risk of cardiovascular events, including subgroup analyses when compared to oleic or n-6 rich vegetable and mixed oils.127 128 129 Furthermore, large prospective studies have found that benefits of fish are only apparent when displacing less healthy foods such as red meat, and that further benefit was found when fish was replaced with whole plant foods (Fig. 1).130 131 132 133 The lack of cardiovascular benefits associated with the consumption of fish oil maybe in part explained by the fact that the majority of marketed fish and fish oils regardless of labelled claims contain high levels of environmental pollutants, such as mercury and PCBs.134 135 136 137 Several studies have found an association between mercury exposure and an increased risk of all-cause mortality, and a recent review elaborated on the numerous detrimental effects of mercury exposure and risk of vascular diseases:138 139

The overall vascular effects of mercury include increased oxidative stress and inflammation, reduced oxidative defense, thrombosis, vascular smooth muscle dysfunction, endothelial dysfunction, dyslipidemia, and immune and mitochondrial dysfunction. The clinical consequences of mercury toxicity include hypertension, coronary heart disease, myocardial infarction, cardiac arrhythmias, reduced heart rate ariability, increased carotid intima-media thickness and carotid artery obstruction, cerebrovascular accident, generalized atherosclerosis, and renal dysfunction, insufficiency, and proteinuria. 

A number of studies have also found evidence of ill-effects of prenatal exposure to mercury from fish on child neurodevelopment.140 Nevertheless, there is suggestive evidence of benefits from long chain omega 3 fatty acids, particularly for those with low circulating levels which could be obtained more efficiently through the consumption of microalgae oil to minimise the risk of exposure to harmful toxins.141

The Primitive Nutrition Series

The following videos (Videos 9-12) are from the Primitive Nutrition Series produced by Plant Positive that address some of the very serious flaws and omissions in Denise Minger's interpretation of the China Study.

Video 9. Primitive Nutrition 62: China Studies, Part I

Video 10. Primitive Nutrition 63: China Studies, Part II

Video 11. Primitive Nutrition 64: China Studies, Part III

Video 12. Primitive Nutrition 65: China Studies, Part IV

The following videos (Videos 13-19) were created as a response to Denise Minger's statements about the Primitive Nutrition Series. In regards to video 16 and the plausibility of removing countries from cross-country comparisons due to the time lag between the war-time decrease in coronary heart disease mortality and the data from 1950 obscuring the diet-heart relationship, Minger correctly pointed out that Denmark did not experience a reduction of heart disease mortality during the war. As previously explained, unlike the other Scandinavian countries, there was no significant decrease in cholesterol rich foods in Denmark, nor was there a decrease in cardiovascular mortality.142

Although the explanation of time-lag may have weakened the diet-heart relationship, the large distribution of mortality rates among countries with high fat intake can largely be explained by differences in availability of saturated fats, which were lower in Denmark, Norway and Sweden. When researchers specifically looked at availability of saturated fat, there were no longer any significant exceptions in the data from the 1950s, with saturated fat explaining almost 70% of the variance of heart disease between countries (Fig. 4).143 Hegsted et al. used a multiple-regression equation using later data and found that almost all variance of coronary heart disease mortality between countries (r=0.92) could be explained by a combination of saturated fat which was positively associated, and polyunsaturated fat and alcohol which were inversely associated with risk (Fig. 5).144

Figure 4. Association of international death rates of coronary heart disease with percentage intakes of total and saturated-types of fat

Figure 5. Mortality predicted by consumption of saturated and polyunsatured fat and all sources of alcohol versus observed coronary heart disease mortality

In regards to the data from the 22 countries, Minger cautioned her readers about interpreting the results of diet and the risk of coronary heart disease and all-cause mortality due to the significant differences in socioeconomic factors between the countries. Less favorable socioeconomic factors are associated with an increased coronary heart disease and all-cause mortality, and would have potentially biased the results towards finding a positive association between plant based nutrients and mortality as it was the developing nations that typically consumed more plant based foods.145 146 147 148 Minger also stated that the GDP per capita for each nation is a 'pretty good way to estimate standard of living'. However, many of the countries with moderate intakes of saturated fat rather than total fat, such as Denmark and Sweden, and higher intakes, such as the U.K and Canada had similar high levels of medical care and GDP per capita, yet the countries with higher intakes of saturated fat had significantly higher mortality rates of coronary heart disease (Fig. 4).149 150

It is not the least bit surprising that while criticizing Ancel Key’s findings in regards to the association between animal based nutrients and all-cause mortality, Minger failed to inform her readers that in the Seven Countries Study prospective study that was not confounded by such significant differences in socioeconomic factors, saturated fat was associated with a significantly increased risk of all-cause mortality in the 10, 15 and 25 year follow-ups.151 152 153

Video 13. "Vegan Propaganda"

Video 14. Response to Denise Minger 1: Scrupulous

Video 15. Response to Denise Minger 2: Not Benefiting from Hindsight

Video 16. Response to Denise Minger 3: Cherry Picking

Video 17. Response to Denise Minger 4: China Revisited

Video 18. Response to Denise Minger 5: Wheat and Carbs

Video 19. Response to Denise Minger 6: Number Needed to Treat

The Fictional Independent Correlation

The cholesterol skeptics frequently cite research that they claim shows no independent association between consuming higher intakes of animal foods and chronic and degenerative diseases by examining these specific foods in isolation, while ignoring what sources of energy these are typically substituted for. These observations are misleading because they ignore the law of thermodynamics where in the general population a decrease of one source of energy will generally lead to an increase in other sources in order to maintain energy balance. In order to provide a more informative analysis of the association between diet and risk of developing diseases, it is therefore essential to study effect of substituting different foods on health outcomes. This was elaborated on in a large research panel organised by Walter Willett:154 155

For example, it may not be useful, as is usually done, to compare a specific food to all other sources of energy, which are usually mainly refined starches, sugars, red meat, and fat-rich dairy products in typical Western diets.

Not surprisingly meta-analyses and systematic reviews that do not compare foods with appropriate alternatives often fail to even find a relationship between refined grains and the risk of cardiovascular disease, weight gain and all-cause mortality, even though it is well documented that replacement with whole grains reduces risk.156 157 While such an over-simplistic approach is apparently sufficient for the cholesterol skeptics to claim that animal foods are safe to consume in almost unlimited quantities, they demonstrate very little interest to judge the health properties of other foods, such as refined grains using the same methods, as doing so would provide little rational for their unfounded claims. Unfortunately this enormous loop-hole has invited a very unwelcome opening for the industries and advocates of fad diets to exploit the medical literature in order to promote the consumption of disease promoting foods. Meta-analyses funded by the associated industries have used this loop-hole to downplay the damaging effects of saturated fat and soft drink consumption, but have nevertheless been refuted by other researchers who demonstrated that the studies that used better methodology found an increased risk of disease.158 159

Studies that focus on substituting food are far more informative and provide increasing evidence for replacing animal foods, particularly red meat and saturated fat rich foods with minimally processed plant foods (Fig. 6).160 161 162 163 164 Note that the definition of whole grains in the studies represented in Figure 6. are grains with at least 25% whole-grain or bran content by weight, permitting up to 75% of the grains as being essentially refined.165

Figure 6. Type II diabetes associated with replacement of other food groups for red meat from repeated dietary data surveys from over 200,000 men and women in the Health Professionals Follow-Up Study and Nurses’ Health Study I & II

The results of many of the referenced epidemiological studies are likely conservative estimates due to imprecise dietary measurement methods that are prone to attenuation bias (regression dilution bias). For example, it is well documented that observational studies significantly underestimate the strong relationship between diet and serum lipids that has been firmly established by hundreds of tightly controlled feeding studies.166 167 168 It was estimated over four decades ago that in order to estimate within 20% of the actual dietary intake, there is a requirement of at least 22 days of 24-hour dietary recalls for a number of macronutrients including saturated fat, and at least 45 days for dietary cholesterol.169 Inaccurately measuring intraindividual variation has been shown to lead to a miss-classification of subjects into ranges of usual dietary intakes, and biasing correlation coefficients towards null.170 Despite excessively referring to epidemiological studies that use some of the most imprecise dietary measurement methods such as single 24-hour dietary recalls as being of 'high quality' or 'good science', the cholesterol skeptics constantly dismiss any epidemiological studies that produce results contradicting their claims as being flawed and entirely uninformative rather than recognising that the results were likely conservative estimates.171 172 

In a recent post Denise Minger discussed a prospective study which found a significant association between higher-protein, lower-carbohydrate diets and an excess risk of cardiovascular disease among Swedish women. She attempted to downplay the study by pointing out the limitation that dietary intake was only measured by a dietary survey focusing on the 6 month period prior to the 16 year follow-up. She suggested that dietary and lifestyle changes throughout the follow-up period may have obscured the results towards finding this excess risk, ignoring the evidence presented by the researchers indicating the exact opposite:173

The long interval between exposure and outcome is a source of concern, because certain participants may change their dietary habits during the intervening period. However, this is more likely to generate non-differential misclassification and, thus, attenuate the evaluated association. In fact, we saw a tendency for the incidence rate ratios to decline with longer follow-up.

Minger also failed to mention the researchers discussion within the paper explaining how the findings from this study were consistent with numerous other prospective studies, including the Nurses's Health Study (NHS) and the Health Professional's Follow-up Study (HPFS) which measured diet up to six times throughout the follow-up period.174 175 176 177 178

The NHS and HPFS are well known for the use of virtually the highest quality dietary measurement methods used in any large scale epidemiological study, including detailed food frequency questionnaires (FFQ) that have been updated every 4 years for over 20 years and validated against multiple-day food records of at least 14 days in a year. A number of cholesterol skeptics have attempted to downplay the quality of the NHS and HPFS, particularly when a recent paper was published describing a significant association between red meat intake and an increased risk of all-cause mortality. They criticised this paper in part due to the variance of dietary intake between the FFQ and the multiple-day food records, clearly ignoring the fact that the researchers found that the association between red meat and excess mortality was actually significantly strengthened in a sensitivity analysis using data from multiple FFQ against the multiple-day food records in order to account for measurement error. Not surprisingly the researchers also found that when compared to multiple FFQ, the association was weakened when using data only from only the single base-line FFQ. Furthermore, no other foods associated with red meat intake could explain this association with excess mortality, and the only nutrients that partly explained this association were those that are naturally found in red meat, including saturated fat, dietary cholesterol and dietary heme. This strongly suggests that the excess mortality was associated with constituents naturally found in red meat, and refutes the claims that the results were obscured by other unhealthy foods associated with red meat intake.179 

Another important factor is that it has been observed that participants often change their dietary and lifestyle habits, including refraining from consuming meat and saturated fat due to illnesses or unfavourable risk factors that ultimately become life threatening.180 This frequently causes researchers to observe participants with a high risk of developing diseases as having lifestyles and consuming diets that are portrayed as being healthy, a phenomenon known to bias the benefits of smoking cessation towards null.181 It is also important not to neglect that many of the recommendations to avoid consuming a number of toxic substances, including tobacco are not based off results from controlled clinical trials investigating hard disease end points, but often purely based off epidemiologic, metabolic and laboratory studies. Ignoring the totality of the evidence simply due to a lack of large clinical trials can result in absurd consequences, including a missed opportunity for healthy longevity.

A Bid Farewell to the Confusionist's

Denise Minger’s biases have become exceptionally clear throughout her posts compromised by very serious and evidently intentional inaccuracies and omissions regarding the evidence supporting the health benefits of plant-based diets. She has also demonstrated her biases through descriptive statements such as ‘How to Win an Argument with a Vegetarian’ and ‘wheat is murder’, as well as with the posting of completely irrelevant photos of vegans that she appears to be ridiculing (Video 13). 

Minger constantly attempts to refute that she is bias in favor of promoting animal foods by claiming that this cannot be true simply because she was previously a vegan, and still eats a primarily plant based diet. Such claims should be considered with extreme caution in light of the fact that a number of other confusionists, including several honorary members of the Weston A. Price Foundation, such as William Douglas and Barry Groves who were opposed to smoking tobacco until they apparently discovered as they have described it, that the consensus that smoking is disease promoting was derived from ‘prejudices based on false science and government propaganda’, that there is a ‘broad spectrum of therapeutic and preventive applications of tobacco smoking for human medicine’, that ‘tobacco smoke contains no carcinogens’, and even that nicotine can ‘Help you live longer’.182 183 184 Perhaps the real reason Minger consumes a plant based diet is simply because she is well aware of the health benefits over a diet rich in animal foods.

Lastly, it is not scientifically justified to assume that someone's diet is optimal just because they perceive themselves as being healthier after a dietary change. Humans simply do not have the ability to feel the initial stages of development of atherosclerosis and cancer, nor feel the cancerous N-nitroso compounds form in their digestive tract and their serum cholesterol rise after digesting an animal rich meal. There is usually a significant time lag of up to several decades between dangerous lifestyle changes and the maximum risk of developing the associated diseases (Video 7).185 186 Furthermore, sudden cardiac death which has been associated with high protein and ketogenic diets is a leading cause of death in the developed world, a disease where there are typically no associated symptoms up until one hour prior to death.187 188 189 190 Dr. Michael Gregor outlines sudden cardiac death in a video regarding the remarkable findings from the China Study explaining how no one needs to succumb to this (Video 20).

Video 20. China Study on sudden cardiac death

Please post any comments in the Discussion Thread.