Storm coming in over Lake Tahoe. Taken from my office window.
Storm coming in over Lake Tahoe. Taken this morning from my office window.

I’ve closed the comments on the last post.  A hundred plus questions is probably enough.
I know the readers of this blog are a clever lot, so I suspect that a number of you will continue to post questions through this post.  Go for it.  I’ll put them up, but unless they are of outstanding merit, they probably won’t get answered.
Now Gary and I have to work on how we’re going to pull this off technically, i.e., whether to go back and try to answer the questions within each comment like I usually do.  Or whether we’re going to do it in a separate post.  Whatever the case, it’s going to take a few days.
A couple of comments.  First, Gary is a science journalist, not a physician or a research scientist.  He is one of the few science journalists out there who can really penetrate the scientific jargon and get to the essence of what particular research papers really mean.  But, due to time limitations, he can’t read every paper on every arcane subject and come up with an intelligent take on it.  He has limited his efforts on the history of how we got to where we are nutritionally, and he has learned the biochemistry and physiology of carbohydrates, insulin and fat storage.  Those are the things he can comment on.  I don’t expect him to spend a lot of time digging into arcane research on issues that don’t have a lot of bearing on those subjects.  That wasn’t our deal.  And, despite my requests for no personal questions, there were a few of the ‘I’ve got this or that problem and am unable to lose weight – what do you suggest?’ variety, which will be ignored.
Thanks for all your interest and the great response.  Hang in there, and we’ll have the answers up as quickly as we can.


  1. Gary: GCBC. Great book! Question: Human beings have been around for over 3 million years and the principle diet was carnivorous, with the exception of the last 10-14,000 years or so when the agrarian/agricultural revolution kicked in. For almost 3 million of those years humankind progressed just slightly or not at all in technological, cultural and philosophical advancement. But the past 100-200 generations have seen an explosion of technological and cultural sophistication not seen for 3 million of those years. Is it possible that the morphing from meat eating to a carbohydrate dominant diet fueled the brain and contributed to this amazing advancement and transformation of the human condition whereas meat eating merely was nothing more than a sustaining physical action and neural activity was muted? Why did this mental explosion occur a few thousand years ago whereas it was non existent for millions of years? Is it diet related and are carbohydrates not the demons that we in the low carb movement see?

  2. Gary,
    Thanks for the great book. I am a physician and have given your book to another physician (my father). Thank you for the great work. It really is a landmark work.
    Is there a vitamin D connection also? There seems to be some evidence that vitamin D increases insulin sensitivity-and may cause weight loss. This could account for seasonal weight gain in the late fall and winter, with weight loss in the spring.
    Thank you

  3. Byron, I think the current view of anthropologists is rather to the contrary. It was the switch of ancient hominids to meat-eating that permitted or fueled the development of much larger brains in comparison to their largely fruit-munching predecessors like the australopithecines. The contribution of agriculture was more likely cultural especially in as much as it encouraged settlement, allowed larger (albeit ultimately malnourished compared with h/g’s) populations and eventually specialization of function. The benefit for cultural development of staying in one place should not be underestimated. The benefit of larger populations is of having more potential for outstanding innovators to arise. Also, the change of agriculture stimulated the development of new solutions to newly arising problems – just as wanting to eat meat stimulated the need for making stone tools all those millions of years ago. I don’t know about you but I don’t think my mental processes are more sluggish just because I eat low-carb.

  4. With respect to a previous poster (Byron Estes), who writes:
    Human beings have been around for over 3 million years and the principle diet was carnivorous, with the exception of the last 10-14,000 years or so when the agrarian/agricultural revolution kicked in.
    How much do we actually know about what humans ate before the agrarian revolution? You say in your book that it is hard to know how much meat people in the US ate on average at the turn of the 20th century. Given how little we know of meat eating habits in recent times, how can anyone say much about what people ate thousands of years and more ago?
    I have heard some people say with confidence that humans evolved to eat meat and other people say, with equal confidence, that humans ate mostly vegetable matter of some kind. I find it hard to imagine that people who study prehistory actually have that much detailed understanding. Do they, do you know?

  5. Thanks for the chance for an additional question!
    In his review of “The Cholesterol Wars: The Skeptics vs. the Preponderance of the Evidence” by Daniel Steinberg, MD, PhD., Chris Masterjohn makes the following statements:
    “Steinberg also suggests that reductions in total fat are similar in effect to reductions in saturated fat. The reasoning seems simple enough — if you reduce your fat intake, some of that fat is saturated, so you will necessarily be eating less saturated fat.
    But the exact opposite is true. The body cannot make polyunsaturated fats but readily makes saturated and monounsaturated fats from carbohydrate. A low-fat diet is low in polyunsaturated fats and effectively high in the saturated fats that the body will make itself.”
    He argues that “saturated fatty acids are not vulnerable to oxidative damage and since it is the unsaturated fatty acids in the LDL membrane that oxidize, we should expect a diet rich in saturated fat and low in polyunsaturated fat to protect LDL from damage. Any benefits from low-fat diets should be seen as benefits of polyunsaturated fat restriction, not saturated fat restriction.”
    Do you agree?
    Chris Masterjohn’s complete review is found at

  6. Two people mentioned heart palpitations when on low carb on the comments to your previous post. Just to save you the trouble of writing this, low blood sugar can cause an adrenalin rush can cause heart palpitations. I suggest these people read up on “reactive hypoglycemia.” This seems to happen to me if I eat too much protein at once, especially for my last meal of the day. My guess is that my liver makes glucose from the extra protein (apparently just because it feels like it) which causes an insulin spike which causes the hypoglycemia.
    A quick test of whether heart palpitations are due to hypoglycemia is to see whether drinking orange juice (or consuming some other high-GI item) makes them go away.

  7. Yes, I have the heart palpitations when in ketosis and drinking OJ or eating fruit alleviates this. Unfortunately, I was identified as reactive hypoglycemic from a GTT by Dr. Atkins during the 1970’s and now as type 2 diabetic, drinking OJ quickly raises blood glucose. Having been an Atkins’ dieter for much of the past 30 years and continually struggling with weight I can without a doubt say that strict Atkins is not the longterm answer for type 2 diabetes nor preventative for those genetically predisposed. While it has kept by blood lipids in a very good range, being forced to measure my blood glucose the past 3 years shows that a ketogenic no/low carb diet ***doesn’t*** equate to consistent lower blood glucose levels. Since my CRP level has been high for years, over 8, and fibrinogen also high (a diabetes complication), I recently started exploring how to lower it before I get all the cardiovascular complications. I’ve incorporated the D’Adamo Eat Right 4 Your Blood Type concepts which for me being AB-, the rarest blood type, means eating NO chicken, beef or pork, much of what I ate to achieve ketosis consistently and assuage hunger. Much of what he lists to avoid is what I pretty much know makes me feel bad. He lists tofu as super beneficial for diabetes for AB- and guess what, blood glucose plummets after eating. Eat a steak, blood glucose rises and stays high. Plus, even in no/low carb ketosis, I still have high blood pressure, below normal testosterone and beginning diabetic neuropathy pains in toes. Since stopping the red meat, pressure has come down. I’ve also introduced high levels of EPA and GLA, turmeric-curcumin and other suppliements that help with inflammation. Even 325mg/day of enteric aspirin has not lowered the CRP. I still stay in ketosis because I feel better overall and it reduces hunger. The diabetes drug, Byetta, causes a similar no hunger feeling and I was able to lose 50 lbs that I gained while becoming diabetic but not realizing it. Also, as has been written by Barry Sears and others, after 6 months, the body adjusts to ketosis and the weight loss stops. Well, I’ve been doing it for 30 years and agree, I don’t lose weight in ketosis and am now diabetic, I lost 60 lbs at age 17 on Atkins, it stopped after 6 months and I have never been able to repeat that feat again on Atkins and I’m currently at 300 lbs. I can’t completely control blood glucose with it either nor my insulin level, currently at 27. Certain higher carb combos, based on D’Adamo, actually lower my blood glucose further than Atkins. For example, oatmeal is super beneficial for AB- diabetics, while I take an initial hit of over 200 blood glucose, after 2 hours I’m around 120. So, while there are many theories out there on no/low/good/bad carbs, when you constantly measure how food affects your blood glucose and other metabolic measurements, then you can see one has to individualize their diet. Hoping I can stabilize this with diet changes but I’m prepared for gastric bypass since that can immediately reverse diabetes due to the reduction of intestine and resulting reduction of certain gut hormones associated with diabetes. Byetta and upcoming newer diabetes drugs look to also affect these hormones.

  8. Thanks to you both for this great opportunity! I devoured GCBC, and I really appreciate also the UC Berkeley lecture and your magazine articles, to which I can refer friends who would find GCBC too intimidating. Looking forward to your new book, Dr. Eades.
    My question also relates to exercise: Can resistance exercise have a beneficial effect on weight loss (as opposed to aerobic exercise), perhaps by boosting overall metabolic rate during the muscle-rebuilding stage, and blunting a starvation-type response to calorie restriction (whether intentional or incidental to lower hunger on low-carb) or would such a boost simply lead to increased hunger?

  9. Gary, do you plan on writing and/or publishing a layman’s version of GCBC? Something which can be read easily by more than just those with the patience and wit to do so perhaps. I must admit that I enjoyed it yet I found it tedious and repetitive in some ways. It dawns on me that this kind of reading is not particularly suited for the masses. Precisely those people who would most benefit from the information it contains. The media would be more open to it as well since it too is composed of people not so well versed on the matter. Then perhaps through the media it would reach many more people than it already did. With a condensed version of GCBC, you’d get another chance at arguing the subject thereby getting more exposure yourself.
    GCBC lite perhaps?
    I for one would buy it in an instant.

  10. I would like to see Taubes answer the arguments Mike (5. November 2008, 9:49 ) made about exercise and weight loss. He gave pretty big list of references and I read some also.
    I also second the idea of a podcast. With 2h mp3 Taubes can address more topics. But also a list of references (to journals) should be written so that we can check the stuff he says.
    Anyway, props to Gary for good work. I am a huge fan and I’m also a information junkie so I am eagerly waiting for this interview to happen 🙂

  11. Gary, Dr Eades,
    I couldn’t resist asking another question. This time, insulin, and its role in fat regulation.
    As I understand it, one of insulin’s key roles is keeping fat stores safely in their place as a a store of future energy – for use when other sources of energy aren’t available. A complete absence of insulin results is zero body fat and loss of muscle/organs – ie, as in untreated type 1 diabetes. A surfeit of insulin results in too much body fat and insulin resistance – the causation of insulin resistance seems to be the subject of much conjecture but it seems that excessive consumption of carbohydrates, too many calories and maybe an inactive lifestyle are factors – probably in that order.
    My understanding is that circulating fasting insulin levels vary in direct proportion to the degree of obesity/fat accumulation. As circulating insulin levels fall fatty acids are released and made available for use as energy at the cellualr level. Is this release of fatty acids incremental and controlled by changes in the balance between insulin and other hormones such as glucogon? Presumably free fatty acids are only released in a proportionate manner – in line with preceived demand for energy. I suspect it wouldn’t be a good idea for 20lbs or more of fat to be instantly dumped in to the bloodstream.
    As surplus body fat reduces do fasting insulin levels fall in proportion, all other factors being equal? From what I have been able to ascertain most men can remain perfectly healthy on single figure body fat percentage, yet many people seem to stall on fat loss in the mid to upper teens or maybe higher, even on very low carbohydrate intake. In your opinion is this because to some extent their insulin resitance is irriversible? Is there a time factor at play: it took 25 to gain weight and attain a certain level of insulin resistance/obesity – it may well take just as long to reduce the insulin resistance/ improve inuslin sensitivity. I don’t know if any studies have been done to examine the possibility of long term insulin resistance on a low carbohydrate diet.
    On a related point you suggest that exercising of and by itself will not lead to weight loss, or put another way, there is no proof that it does. Do you, however, think that it can contribute to reducing insulin resistance by improving insulin sensitivity and reducing insulin resistance? Some people seem to think that weight training and interval training can play a role here?
    As I understand it measuring insulin resistance is extremely difficult, and assessing differences in insulin resistance between say muscle, fat cells and liver cells is even more difficult, and expensive. I suspect other cells may also develop insulin resistance – nerve cells for example as well. Is it possible that a lower carb diet may reduce insulin resistance at the level of the fat cell, whereas weight training or anaerobic exercise may reduce the insulin resistance of muscle tissues and perhaps of the liver. And perhaps loss of body fat can improve insulin sensitivity across the board.
    I would be interested in your view on this. You hit in GCBC that for some a low carb approach offers improvement but not necessarily a panacea for obesity and presumably insulin resistance. Is that because its what’s the evidence you have come across suggests? Do you think this is an area that warrants further research?
    Paul Anderson

  12. Hi Gary. I’m an Exercise Physiologist from Spain, where nutritionists are very conservative and I allways wonder why. Your book finally explained that. I have to say that you did an absolute superb work and you should be rewarded for it. Congratulations!!!
    Without further delay, let’s go for the question:
    Kallio et al published a study, where they showed that a low-insulin-response diet down-regulated hormone-sensitive lipase (HSL) [1].
    And, Sandra L Salsberg and David S Ludwig say in the editorial [2]:
    “HSL, a key enzyme in the release of fatty acids from adipose tissue, has been proposed to affect body weight and metabolic variables. Mice made deficient in HSL by genetic manipulation are resistant to genetic- or diet-induced obesity (4, 5). Women carrying an allele associated with decreased HSL activity have lower fasting and simulated insulin concentrations, and men with this allele have lower nonesterified fatty acid concentrations (6). In light of these data, proteins involved in lipolysis have become targets of drug development for the treatment of obesity and the metabolic syndrome. Thus, decreased HSL activity might mediate some of the purported benefits of diets designed to lower insulin secretion. “
    Nevertheless, I learned in Physiology that Adipose lipoprotein lipase (LPL) activity is increased by insulin, and HSL decreased, which is way people with hyperinsulinemia tend to gain fat, and have trouble loosing it.
    In fact, CLA (a weight loss supplement) works by inhibiting LPL and increasing HSL activity.
    But I know that people with the metabolic syndrome, despite having hyperinsulinemia, have high HSL activity (which is what Kallio et al , Sandra L Salsberg and David S Ludwig are saying) which leads to an elevation of triglycerides (which can also happen with CLA in Metabolic Syndrome Patients).
    Given this, how can hyperinsulinemia lead to fat gain in metabolic syndrome patients????
    On another note, Metabolic Syndrome, abdominal obese patients have insulin resistance, but is it at the whole body level (liver, muscle, and adipocyte), or only at the muscle and liver? Because if it is at the whole body level, then how can insulin lead to lipogenesis?????
    1) Kallio P, Kolehmainen M, Laaksonen DE, et al. Dietary carbohydrate modification induces alterations in gene expression in abdominal subcutaneous adipose tissue in persons with the metabolic syndrome: the FUNGENUT Study. Am J Clin Nutr 2007;85:1417–27.
    2) Salsberg SL, Ludwig DS. Putting your genes on a diet: the molecular effects of carbohydrate. Am J Clin Nutr. 2007 May;85(5):1169-70.
    Many thanks

  13. 1. In your opinion, what would be the most significant thing(s) the new administration could do to reverse the current state of diet & health policy, dogma, and common “understanding”?
    2. Do you have thoughts on the diet-emotional/mental health link and the effect of low fat/high carbohydrate and calorie-restricted diets on America’s emotional and mental health?
    3. Given the truth of the theory of diseases of civilization being due to elevated insulin due to high levels of refined carbohydrates in the diet, what is the potential public health impact of refined carbohydrates vs. tobacco?
    4. Given our litigious culture and the success of actions against “big tobacco”, when will individuals and state attorney generals begin suing “big carbo” (quasi-government American Heart Association, American Diabetes Association, Center for Science in the Public Interest, pharmaceutical and processed food industries) for damages and health-care costs?
    Congratulations on writing a significant book. Thank you for your effort!

  14. Mr Taubes or Dr. Eades,
    Have you any opinion on juicing? I generally juice 2-3 cups of carrot juice, sometimes containing apples, oranges, parsnip beats.

  15. Oh, and here’s a 5th one –
    5. Remembering your quote about the heart-healthy meal being the porterhouse steak, not the baked potato or whole-grain roll, and given the possible role of elevated blood glucose and insulin in the survival and growth of cancer cells – Care to comment on the percieved “safety” of organic foods (including organic junk-foods) and the possible implications upon the organic movement (remember Robert Rodale?)?

  16. hey, I bumped into Gary himself today at Fred’s studio, didnt have any time to ask any questions tho, heh heh…

  17. I, like Byron (the first commenter of this post), would like to know Gary’s thoughts on anthropological evidence that supports human evolution based on low-carb diets and whether or not an increase of dietary carbohydrate influenced history profoundly. I’m speaking of soley of physiological changes (i.e. more glucose available to the brain = more mental drive for faster social/cultural development).
    As previous commenters pointed out, there is no doubt that more carb foods in the diets of population groups allowed for a more sedentary life and a reliable source of food. But this theory still doesn’t address the changes that may have occurred in the psyche and bodies of these population groups to influence, for example, empire building and the worship of complex dieties.
    So, in short, the question is: In human evolution, did a dietary increase in carbohydrates influence a desire for bigger/faster social and cultural growth? Is this continued increased consumption of carbs what drives our “gotta have it now” culture today? Please speak mainly from a physiological perspective.
    Oh, and thanks for writing such a wonderful book!

  18. To Beth re: meat-eating and evolution …
    It’s a very safe bet to say that our human ancestors were meat-eaters due to studies of modern hunter-gatherer population groups — such as the Inuit, Masai, and aborigines of Australia.
    Also, we must remember that meat/fat has the highest caloric return for energy output, as Cordain states. It’s a lot easier to let the animals eat the plants — then we eat the animals! Our ancestors, in constant survival mode, would have chosen this most efficient approach to nourishment.
    Lastly, animal populations in pre-agricultural times were far greater than those of today. Their sheer numbers would suggest that humans took advantage of this plentiful and nutritious food source.

  19. One thing that was striking to me about GCBC is that it primarily addresses the sedentary population or at best the “acquainted with the treadmill a few times a week” population (which makes sense, since that describes the majority of Americans and no doubt the majority of study populations drawn from the American public). However, I’m interested in whether Mr. Taubes came across any material more relevant to an athletic population while researching his book, particularly athletes in activities other than endurance sports (e.g. team sports, sprinters, etc.) — I think the studies discussing low-carb endurance performance have been pretty well covered in the blogosphere. If he had any educated analysis to share that would be great, but raw citations would also be awesome.
    I’d also be curious about whether Mr. Taubes has any gut feelings (or informed opinions) on whether phenotype or activity pattern makes more of a difference to those people who feel and/or perform better on higher or lower carb macronutrient ratios.

  20. In response to Byron and others:
    Carbohydrates as a macronutrient had nothing to do with increased “brain power.” There isn’t any magical power that carbohydrates hold to turn us from brutes into geniuses.
    Civilization occurred from Hunter-gatherer tribes because of sustained population explosion. Population explosion was generated by growable carbohydrates, ie agriculture. It led to a massive increase in consumable calories. Previously, as a hunter-gatherer, human population was extremely limited because of available calories. If they didn’t kill it or gather it, they didn’t eat it. Rather, they starved.
    Hunter-gatherers were simple folk. They didn’t need technology or the “advances” of civilization because they had all they needed. It’s how humans evolved. It worked for us.
    Contrast that with civilization – now that you have agriculture, you need technology and written language to construct and regulate irrigation, calendars and mathematics and astronomy to estimate crop harvest times, crop yields, etc. People don’t have to actually go out and kill animals anymore, because there is plenty of food. The civilized people were free to specialize into a role that was needed.
    It was agriculture and the transformation of the human from hunter-gatherer to civilian that caused the rapid advance of technology and “brain power.”

  21. One more comment on heart palpitations for people who combine low-carb eating with the consumption of alcoholic beverages.
    It has been known for years that alcohol consumption temporarily prevents gluconeogenesis, e.g., the production of glucose by the liver. This process, is, of course, an especially important backup system for keeping blood sugar in normal ranges for people on a low carb diet. The low-carber is thus more likely to experience low blood sugar -> high adrenalin -> heart palpitations after consuming alcohol.

  22. If calories are not the issue and carbohydrates, by virtue of their effect on hormonal tone are the main cause of obesity, would eating 1,000 calories more than your base metabolic rate of pure fat meat cause fat gain?

  23. It’s been a long time since I have seriously studied human paleontology (grad classes about 25 years ago), but I’d like to add that it’s amazing how much can be determined regarding diet based on studying the dentition of human fossils.
    The size, shape, and wear patterns of the teeth can show whether the diet of the specimen was primarily hard seeds and vegetable matter that needed to be ground up before being eaten, as opposed to different patterns that are evident in meat eaters.
    It’s good to study modern-day hunter-gatherers and then try to extrapolate what early humans ate, but it’s the dentition that really tells the story.

  24. What would cause a person with reactive hypoglycemia to progress on to type II diabetes even while doing extremely low-carb? Eating too much protein? Eating too often?
    None of the things mentioned should cause the problem. I would suspect a problem with the beta cells themselves.

  25. Stargazey,
    May I suggest you read Jenny’s excellent Blood Sugar 101 site? She has a lot of info on the multiple causes of diabetes that have identified (and unidentified but suspected) and lumped into the catch-all term “Type II”.
    Some folks don’t have type II at all, but later and slower developing forms of Type I and 1.5 DM. Often their doctors don’t even know the difference, especially primary care doctors who are not up to date and still using what they learned in medical school. There are different treatment protocols for some of these “not really II” types so it’s important to to have the underlying reason for the diabetes identified to get the right treatment.
    www dot bloodsugar101 dot com (replace dot with . and remove the spaces)

  26. Well this one is tad bit late but here goes:
    Would Gary research in a future project the science behind cancer? The chapter in the book is interesting but I wonder what he can achieve if he puts the same kind of effort as that in obesity and heart disease.
    I find the way cancer is handled by the medical community mind-baffling: everything that is done weaken the immune system tremendously to the point that I’ve wondered did the people I know who died of cancer, really die from it or from the mind boggling array of drugs and industrial strength pain killers?

  27. Dr. Davis at the Heart Scan Blog writes this, as he is listing ways to reduce C-reactive protein levels:
    “–Not allowing saturated fats to dominate–Yes, yes, I know. The demonization of saturated fat conversation has been largely replaced by the Taubesian saturated fat has not been confidently linked to heart disease conversation. But controlled feeding studies, in which a single component of diet is manipulated (e.g., saturated vs. monounsaturated vs. polyunsaturated fat) have clearly shown that saturated fats do activate several factors in the inflammatory response.”
    A response?
    I disagree. It’s a question worthy of a post versus a comment response.

  28. Saturated fats can increase inflammation, but this is an indirect or transient effect. PUFAs are the main cause of inflammation – eating a lot of them or having a lot of them in your body will make you more vulnerable to damage by pollution, toxins, stress, etc. Saturated fats make the body stronger and more resistant to disease. They are falsely demonized. Long-term studies I have seen show that saturated fats reduce mortality from poisoning, various chronic diseases, asthma, and other auto-immune diseases. The fear of saturated fat is misplaced. We should be afraid of PUFA vegetable oils and foods that contain large amounts of them, like farmed fish, excess nuts and seeds, conventional chicken and turkey, etc.

  29. Also, a lot of the confusion comes from bad terminology. For example, when you ask someone what is a “saturated fat”, they will say coconut oil, cocoa butter, beef, butter, pork, chicken, eggs, and turkey. But those range from ~2% PUFAs (beef) to 23% PUFAs (chicken). So, you get conflicting results. PUFAs are definitely dangerous. PUFA oils like sunflower increase cancer a lot, even at low intakes like 3% of calories. Fats like chicken and turkey skin may have a similar toxic effect at say 10-15% of calories. Beef and coconut oil protect against cancer, unless the diet is supplemented with PUFA oils, as Taubes noted. Here’s a review paper.
    “In further studies, Carroll and Hopkins (3) demonstrated that
    diets containing 3% sunflower seed oil (polyunsaturated fat) and
    17% beef tallow or coconut oil (saturated fats) enhanced tu-
    morigenesis as much as did a diet containing 20% sunflower
    seed oil. Rats on these diets developed twice as many tumors
    as those fed diets containing 20% of the saturated fats alone.
    These observations suggest that there may be a requirement for
    polyunsaturated fat in mammary tumorigenesis, which is not
    satisfied by fats such as coconut oil or beef tallow, but can be
    provided by adding 3% sunflower seed oil to diets containing
    these fats. A recent paper by Cave and Jurkowski (6) also
    showed that when the polyunsaturated lipid content (com oil) of
    the diet fell below 3% there was a decrease in tumor incidence
    in rats treated with W-methyl-W-nitrosourea. It is thought that
    linoleate may be the essential fatty acid primarily responsible for
    the tumor-promoting effect of unsaturated fat (14).”
    My conclusion is that the typical American / Western Diet, high in PUFAs, causes disease. If PUFA oils are eaten at all, then you should avoid meat, eggs, dairy, etc. Conversely, if you’re eating meat, eggs, and dairy, then PUFA oils should be eliminated. They are prevalent in the processed foods Americans eat, as well as mayonnaise, salad dressing, most cooking oils used in restaurants, etc. I would focus on red meat, dairy, tropical oils (coconut and macadamia), small amounts of olive oil, wild ocean-caught fish, etc.
    Although I agree with your conclusions, I wouldn’t put a whole lot of stock in the study you referenced since it was a rat study. I didn’t pull the study and read it, but certain strains of rats can develop tumors at the drop of a hat when given substances that don’t affect humans at all.
    Having said that, though, I do completely agree that vegetable oils should be avoided at every turn.

  30. Human studies have shown similar associations with PUFAs and disease. Chris Masterjohn has written about the China Study and debunked T. Colin Campbell’s conclusions. What the China Study really shows is that the more PUFAs and the less SFAs eaten, the more atherosclerosis progresses, whereas a high-SFA and low-PUFA diet reverses atherosclerosis. Also, the Chinese eat hardly any refined sugar (as Taubes noted). This is why the low-fat proponents have been brainwashed. They get people to eliminate vegetable oils and refined sugars and grains, along with animal fats. Then they claim that the reduction of fat was the key factor. They never go by the scientific method. They change several variables at a time.
    There seems to be a deadly synergy between a high-fat, high-PUFA, and high-carb diet, esp if refined sugars are the main source of carbs. John Yudkin and others have noted that refined starch is a lot less harmful than refined sugar, calorie for calorie. Most people now eat huge amounts of PUFA oils (soy, corn, flax, safflower, cottonseed, canola, peanut, sunflower, rape seed, walnut, hempseed, etc. Plus, lots of refined sugar too. This diet is a disaster that only causes gradual degeneration and one chronic disease or another.

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