Obesity – How and Why Did We Get So Fat?

Obesity - How and Why Did We Get So Fat?

The modern history of coronary heart disease is quite remarkable. Acute myocardial infarction (acute heart attack) appears to have been relatively uncommon until it emerged in the early 1920s. Then came the plague.

In the 1950s coronary heart disease had become the most common cause of death in the industrialized world. The symptoms were often dramatic and devastating. A previously healthy person was hit by sudden excruciating chest pain, often associated with cardiac arrest and sudden death. The survivors often had damaged heart muscle, sometimes resulting in heart failure, severely compromised quality of life and a shortened life span. Coronary heart disease had become an epidemic. A major threat to public health worldwide.

In Europe and North America, the death rate from coronary heart disease reached a peak in a 15-year period between 1965 and 1980. Since then it has dropped dramatically. A 50-80% decline in mortality has been reported by many countries between 1980-2005, and the decline appears to be continuing (1,2). However, the burden of disease remains high, partly due to the aging population.

Available evidence suggests that the mortality decline is due to decreased incidence of coronary heart disease as well as better prognosis of those affected. In other words, there are fewer new cases and those affected live longer.

However, explaining these remarkable results has proven difficult. The question is whether the management of risk factors such as high blood cholesterol, smoking, and high blood pressure has been so successful or if it is the treatment that has improved?

Many researchers have used the IMPACT model (3) to examine the contributions of various factors to the decrease in death rate from coronary heart disease. This statistical model incorporates known major risk factors for coronary heart disease as well as currently used medical and surgical treatments.

IMPACT has been used to explore the contributions of risk factors and treatments in over 15 countries where mortality rates have been declining, including England, Wales, Scotland, Finland, Sweden, Italy, Spain, Iceland, Northern Ireland, New Zealand, USA and Canada. The main results of these studies suggest that approximately 40 – 75 percent of the decline in mortality is attributable to reductions in risk factors. The biggest achievement is due to reductions in total cholesterol, smoking, systolic blood pressure and physical inactivity.

Nobody will deny that from a public health perspective, these results are very impressive. The declines in smoking and saturated-fat intake and better treatment of high blood pressure are believed to be a consequence of important public health and primary care interventions (4).  Obviously, great achievements have been made. So, is it time to celebrate?

The Uninvited Guest

In fact, we’ve been partying for some time now. Between the clinking of glasses and through our blurry vision, we’ve slowly discovered an uninvited guest. The intruder looks familiar, but we can’t recall where he came from or how he managed to slip through the backdoor. Or maybe he just strolled through the main entrance.

Today this intruder is a major celebrity. Everybody’s talking about him and we spot him regularly on the front page of major newspapers and magazines; television shows can’t get enough of him, and today scientists and public health experts consider him the biggest threat to public health worldwide.

Although we can’t seem to agree on the why’s and how’s, we’re suddenly confronted by a pandemic of obesity.

Many of the studies that used the IMPACT model found that the positive results were partly offset by increases in body-mass index and prevalence of diabetes, both accounting for an increased number of deaths from coronary heart disease.

A few months ago we saw an interesting and quite scary report on the global, regional and national prevalence of obesity (5). The worldwide prevalence of overweight and obesity combined rose by 27.5% for adults and 47.1% for children during the past three decades. These increases were found in developed and developing countries.

There is no reason to believe that the obesity pandemic and the consequent increase in type 2 diabetes will not adversely affect the progress made regarding the declining mortality from coronary heart disease. On the other hand, obesity may not necessarily increase the relative contribution of cardiovascular mortality because obesity is also a risk factor for other serious illnesses, such as many types of cancer and Alzheimer’s disease.

The Univited Guest

Why and How Did We Get So Fat?

But how did this happen? How did we get so fat and metabolically sick in such a short time?

Although explaining the large increase in obesity is complex, one thing is certain; We’ve managed to create an obesogenic environment.

Most commonly, increased calorie intake and lack of physical exercise are considered the two most important contributors to obesity. But such a simple explanation is unlikely. The composition of the diet may be important as well.

Interestingly, obesity has increased in many countries at the same time as the intake of dietary fat has decreased. Most likely added sugar is partly to blame, at least in some areas of the world. In fact, the role played by sugar-sweetened beverages in the obesity epidemic is a matter of great scientific, clinical and public health interest.

Today public health experts believe that the success achieved in reducing fat consumption, saturated and trans fats in particular, has resulted in lowering of blood cholesterol in most industrialized countries. This is by many considered the main reason why the death rate from coronary heart disease has declined so rapidly.

Many experts worry that the recent increase in fat intake resulting from the popularity of carbohydrate-restricted high-fat diets may trigger a new epidemic of coronary heart disease.

However, one can’t help wondering whether the current obesity epidemic is a trade-off for lowering blood cholesterol in the population.

The widespread promotion of low-fat diets in the 1980s and 1990s led to a reduction in the percentage of calories from fat in the United States and many other countries. At the same time, the consumption of calories from carbohydrates increased.

Despite these dietary changes, the prevalence of obesity and type 2 diabetes continued to rise (6).

Or should we put it differently; Because of these dietary changes, the prevalence of obesity and type 2 diabetes has skyrocketed and become a threat to public health.

Although increased carbohydrate and reduced fat consumption may have lowered total and LDL cholesterol (the bad cholesterol), there are some serious concerns. High-carbohydrate diets reduce HDL cholesterol (the good cholesterol) and raise blood concentrations of glucose, insulin, and triglyceride and blood pressure, contributing to the now well-recognized metabolic syndrome, sometimes called insulin resistance syndrome, that is known to increase the risk of coronary heart disease and type 2 diabetes.

If public health authorities claim their interventions made an important contribution to lowering coronary heart disease mortality, their interventions or lack thereof may be responsible for the pandemic of obesity. It happened on the same watch, didn’t it?

It is time public health authorities critically evaluate the consequences of the dietary recommendations of the last thirty years. Needless to say, the effects on the food industry have been astonishing. For years, low-fat products have been highlighted as a symbol for good health. Everything that possibly can raise blood cholesterol is associated with danger. Dairy fat, eggs and red meat have been demonized.

Although we can certainly allow us to celebrate our success in preventing and treating coronary heart disease, it’s time to face the darker side. Obesity and diabetes are the new threats. It’s time to meet with the uninvited guest.

22 thoughts on “Obesity – How and Why Did We Get So Fat?”

  1. Excellent summary Axel. I’m reminded about the saying: half of what you learn in medical school is wrong, you just don’t know which half. It’s becoming more and more apparent that we’ve been demonizing the wrong food group for decades now. The only “bad” dietary fat is trans fat, and the real villains are almost certainly processed carbohydrates and massive consumption of added sugar.

  2. For most of my life I’d be screaming that the government and health authorities should get to it and educate the public. Unfortunately that doesn’t seem to work, they just got it all wrong, people suffered and now so entrenched in wrongness they are afraid to do a 180.

    People need to educate themselves, take the path that seems right and get ready to change if it isn’t working for them. Some of us have done that and succeeded so far. Put all the info out, tell the people we don’t really have a clue and let them choose.

  3. Why do all doctors , including you Axel, seem to assume that the phrase ” risk factors” means ” causes” . In my opinion it’s one of the reasons we’re in the mess you describe.

    What if all the risk factors for heart disease are in fact symptoms of heart disease or even symptoms of the real causes of heart disease, and do not in any way cause it? That might even include obesity? Why is this reverse causation always discounted?

    Have you considered that the epidemic of syphilis in the early 1900s may have caused the epidemic of heart disease, or that the stress of two world wars may have had an effect? Who’s to say that it really had been saturated fat causing heart disease. Not recent meta studies !

    • Hi David.
      I don’t think or assume that “risk factors” means “causes”. I’m well aware of the difference between correlation and causation.

      However, there’s evidence that modifying risk factors affects disease risk. For example, abstaining from smoking reduces the risk of cardiovascular disease and so does treating high blood pressure. Furthermore, there’s evidence that lowering cholesterol may affect risk, particularly in secondary prevention.

      I’m glad you bring this up David because it’s important. For example, I don’t think the increased risk associated with obesity is associated with body weight by itself but rather all the problems that travel with obesity, such as inflammation, diabetes, lipid abnormalities, inflammation etc.

  4. “High-carbohydrate diets reduce HDL cholesterol (the good cholesterol) and raise blood concentrations of glucose, insulin, and triglyceride and blood pressure, contributing to the now well-recognized metabolic syndrome, sometimes called insulin resistance syndrome, that is known to increase the risk of coronary heart disease and type 2 diabetes.”

    Playing Devil’s advocate here, aren’t there many Dr’s out there (Ornish, McDougall, Esselstyn) who have both advocated and lived these high carb diets and who have had excellent results in reducing all the very things you say high carb diets do?

    If we’re going to talk about carbs that do damage, why not mention that it’s primarily refined carbs with high GI’s that cause this? Seems to me that carbs become inherently bad, only once they’ve become “westernized” and processed and loaded with other rubbish.

    • Of course you’re right Bill. There are certainly good and bad carbs. Obviously the best option would be to choose good carbs and good fats. In fact, that’s not very complicated.
      However, it appears the low-fat mania has driven the food industry to market not only good carbs, but also products loaded with fructose and refined carbs. The sugar content of many low-fat food products is a good example.

      • “However, it appears the low-fat mania has driven the food industry to market not only good carbs, but also products loaded with fructose and refined carbs. The sugar content of many low-fat food products is a good example.”

        On this, we’re in total agreement. I think that real food, either from animals or plant based is the way to go. I’m still not sold on the recent praising of saturated fats but that’s just because of the way they affect my own lipid profile but if it works for others, have at it. Just make sure we’re all eating real food.

    • As far as I know the Ornish et al type diets are high in fiber and low in “cheap” carbs, which would alter the microbiome. It would be interesting to see an analysis of “Ornish poop”. It might even be that these diets are in fact high fat since the gut bacteria could digest the fiber into short chain fatty acids.

      In fact most of the risk factors could be gut related. Even smoking (and quitting) changes the makeup of gut bacteria.

  5. Hi Axel!
    Great summary. The diabetes and obesity epidemic is becoming the major public health issue of the 21st century along with other chronic non-communicable disease. This is a global problem. I think you are absolutely right in that the low-fat diet agenda is probably a major player here as well as lack of physical excersise. Why then did the mummies of Egypt have signs of atherosclerosis when they died at age 35 some 3 thousand years ago? Probably because they were infested with parasites and had secondary chronic inflammatory state despite their high standard of life. They never made it to middle age and died from infection or injury. So, maybe the intruder in the party has many faces and changes from one time to another and from one region to another. Our epidemiological studies date back some forty years and we know very little of the mechanisms of disease before that. We know that if you replace saturated fat with carbs you gain nothing in terms of CVD. If you replace saturated with polyunsaturated fat you will succeed. However, unfortunately very few people do. People only read the headlines and don´t get the whole message. That´s why we need people like you! Keep up the good work.

    • Thanks Karl.
      You raise some interesting points. Our epidemiological research is in fact very young and we often tend to look only at the present. We probably need a much wider perspective as I believe you’re implying.
      Appreciate your comment.

  6. Another objective, well thought out doc’s opinion founded in facts.

    I think the medical-scientific community has missed the uninvited guest. Many can’t see the food industry combining with the medical community to increase our carbohydrates and decrease our fats while adding a few very bad elements into ouf foods. Any RN knows that too many CHO’s lead to DM and treatment is the control of CHO’s.

    My husband just got his latest blood tests back. His HDL is the highest it has ever been! 57. Trigycerides are the lowest ever at 111 and CRP .5. These numbers in the past have been awful while on low fat diet and statin. HDL as low as 32, Triglycerides as high as 1200! CRP 8. He’s off his meds eating saturated fats, almost no carbs and off all scripts. BP now runs around 115/70 except when he’s upset with me! He feels better than he has for years and between the 2 of us we’ve lost 70 pounds! *Oh, he just built 2 horse stalls for my horses this summer! He just retired.

    At 69, we plan to stay physically active and healthy, watching for the signs of our ancestral diseases. So far so good. Life is great!

    My health blog: https://time4health4tannngl.wordpress.com/2014/11/21/our-latest-milestones/

    I so appreciate this blog. And I learn a lot just reading the comments!

  7. Doc,

    I am very glad that you formulate your views based on actual facts. CHD mortality has indeed been massively reduced in Western world and the single most explanatory factor that explains this positive change is reduced cholesterol levels that were followed after people reduced their intake of animal fat. However, we didn’t get fat because of carbs, that is were you are being subjected to flawed reasoning. The Americans in particular got fat at the same when farm work was largely mechanized and when walking roads were eradicated from the suburbs.

    I am glad to see that real expert also partook in the discussion followed by the article ob BMJ:

    “In formulating his views regarding conventional wisdom relating to saturated fats Dr Smith appears to have been strongly influenced by a number of popular books most written by lay authors, and examination of several original publications1. Lay authors may not understand the inherent complexities, imprecisions and inaccuracies associated with individual studies and, whether by design or simply because they have not carried out a formal search of data bases, may not be in possession of the totality of evidence. “Cherry picking” of evidence whether by design or default can lead to serious misinterpretation of existing knowledge

    Two examples taken from Dr Smith’s feature serve to illustrate how individual studies may be misinterpreted. Dr Smith describes the Women’s Health Initiative (WHI) as “the biggest test of the saturated fat hypothesis”. This is incorrect. The saturated fat hypothesis assumes that the effect of this nutrient on coronary heart disease (CHD) is to a considerable extent mediated via cholesterol. In the WHI the low fat intervention only achieved a 0.09 mmol/l reduction in cholesterol which would not have been expected to achieve a reduction in CHD2.Furthermore the lower fat higher carbohydrate was associated with a small weight loss compared with the usual diet, a finding consistent with a systematic review of all intervention studies of lower fat diets. The fallacious ecological argument that Smith invokes to infer that lower fat intakes in some countries have led to increasing rates of obesity could be applied equally to the opposite phenomenon in China (18% of the world’s population) where the increasing fat intakes correspond closely with rising obesity rates3.

    The Hooper et al. Cochrane Collaboration systematic review has also been misinterpreted4. The 14% reduction in cardiovascular events associated with a reduction in saturated fat is what might have been expected on the basis of the expected reduction in cholesterol5. This would translate into appreciable public health benefit. No benefit was observed in terms of mortality but nor would this have been expected given the relatively short duration of the intervention studies4.

    Systematic reviews also differ in their findings based on how the research question as well as the qualifying criteria for inclusion of studies is defined. This opens the door for cherry picking of results, as is often seen in the popular press and, unfortunately, some academics who are not trained in nutritional science or who may have vested interests. Systematic reviews have shown the importance of limiting saturated fat in favour of MUFAs and PUFAs 4, 6, 7 but approaches and interpretations differ8.

    Dietary guidelines developed by authoritative bodies around the world (e.g. by World Health Organisation and national governments) are based on careful and systematic reviews of the literature, the type recommended by the Cochrane library9-11, and are derived through processes such as those outlined by GRADE12. The guidelines lead to the conclusion that a wide range of dietary patterns (and macronutrient compositions) are consistent with a healthy diet. However, they are consistent in their advice to limit intake of saturated fat in favour of mono and poly-unsaturated fats, and limit sugar and highly refined carbohydrates in favour of wholegrains, fresh fruit and vegetables. Or, in the words of another popular author “eat [whole] food, not too much, mostly plants”13.

    Sincerely
    Rachael McLean, Murray Skeaff, Jim Mann and Lisa Te Morenga”

    • Thanks Richard

      There are more responses to Dr. Smith’s article in The BMJ than the one you’ve pasted into your comment. I guess some are from real experts and other from not so real experts. Here are all the comments if someone’s interested.

      Merry Christmas

  8. Yes,

    god jul, Doc.

    The only experts who partook in the debate were obviously you and McLean & Co. Your ideas in regards to SFA and LDL go against those embraced by pretty much every single publicly financed body dealing with public health. To put things into perspective, you are like few evangelic christian evolutionary biologist who are against evolution theory and thus at odds with scientific community and consensus.

    • ^Well actually, I need to take back my words. You seem to have somewhat changed your view on LDL and SFA lately. Now the story is that SFA reduction indeed saved lives, but it was a wrong message because the advice to reduce SFA is causally related to the fact that people have gained weight during the last decades.

      I disagee, see the article by Obesity scholars Bray & Popkin. If there’s one macronutrient that makes as fat, it’s surprise….fat.

      Dietary fat does affect obesity
      https://ajcn.nutrition.org/content/68/6/1157.full.pdf+html

      The lesson from China is bullet-proof, when you have population eating very low-fat, high starch diet, as was typically consumed in rural, undeveloped parts of the world, body weight-gain is largely mediated via fat intake. Moreover, the easiest and quickest way to make lab animals fat is feeding them high-fat diets. See also the interview by 1 one the fathers of diet-heart, Jeremiah Stamler:

      There’s More Work to Do for Longer Lives and Better Health
      https://www.nytimes.com/2005/08/23/science/23conv.html?pagewanted=all&_r=0

      • “Dietary fat does affect obesity.”

        Yes it does. But which is more important; the amount of fat or the kind of fat? If kind of fat is a deciding factor in obesity, it makes sense to inquire as to which types of fat have proliferated in lock step with the obesity epidemic. Excerpt from a article entitled A high fat diet rich in corn oil reduces spontaneous locomotor activity and induces insulin resistance in mice:

        “…in recent years, to protect against chronic diseases, saturated fatty acids have been extensively substituted with unsaturated fats like monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA) in western food supply. For example, in Canada, increases in dietary fat content over last century are attributable almost entirely to increases in MUFA and PUFA, whereas saturated fat has remained constant.”
        https://www.jnutbio.com/article/S0955-2863%2814%2900247-2/abstract

        Barry Popkin notes that the increase in vegetable oil is global.

        “If you go back to those same villages or slum areas today…their diet includes a lot of vegetable oil… In China…Rice and flour intake is down, and animal-source foods such as pork and poultry and fish are way up, and the steepest increase is in the use of edible vegetable oils for cooking…People are eating more diverse and tasty meals; in fact, edible oil is a most-important ingredient in enhancing the texture and taste of dishes…The edible-oil increase is found throughout Asia and Africa and the Middle East as a major source of change.” https://articles.orlandosentinel.com/2003-09-28/news/0309270148_1_overweight-or-obese-women-were-overweight-south-africa

        From the American Heart Association:

        “Contemporary changes in diet (including increased caloric content, increased consumption of glucose and omega-6 fatty acids, decreased consumption of omega-3 fatty acids) and an overall decrease in exercise and activity have contributed to an increased incidence of obesity and diabetes in the adult and pediatric population. These trends, in turn, have led to an increased incidence of cardiovascular diseases including atherosclerosis, AF, and congestive heart failure, each of which is associated with increased risk of mortality. SCD (sudden cardiac death) due to arrhythmias is a primary cause of increased mortality.”
        https://circ.ahajournals.org/content/116/10/e320.full

        We see, then, that it is widely acknowledged that omega-6 consumption has increased but only a handful of researchers have studied the effects of this change.
        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3076650/

        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3889814/

  9. ^I like very much the 1970s low-fat philosophy as cornerstone for healthy eating, the kind of diet promoted by Pritikin/McDougall, the starch-based approach. The key for optimal health is in potatoes, barley, oat and rice.

    Yet, we have compelling evidence that feeding corn oil great quantities to sub-human primates can effectively lower cholesterol and reverse heart disease. We also have some preliminary evidence on positive effects of the high-fat vegan “Eco-Atkins” diets. Yet, the problem with fat is that it makes us easily fat. Feed the Mediterranean diet to a person who has been exposed to the Ornish diet for a long-time and that person almost certainly ends up gaining weight, no matter what is the baseline weight. I don’t think it would be a good idea to put people who have grown up on the traditional, starch-laden Okinawa diet on experiment with the Mediterranean diet.

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