2016 Edited to Add: When I first began writing here I generated a searchable database for references and I have since done away with that option. This entire series remains to be edited to include the full references within each piece. As time allows, this series will be edited to include complete references at the end of each part in the series.
As a refresher for the series so far, Part I laid the groundwork for why human beings in particular are not only born with a lot of fat, compared to other land animals, but they need that fat for brain development as they grow. They also need fat to maintain brain function throughout life.
Whether our ancestors were actually aquatic or shore-dwelling, it is clear that one of the environmental advantages of being in or near the water was a ready supply of food stuffed full of essential fatty acids.
In Part II, we looked at some of today’s environmental pressures that actually compromise our ability to continue relying on those sources of essential fatty acids. Part II also covered our modern issues of massive human populations thanks to the discovery and use of petroleum; it reviewed heavy over-fishing and trophic cascades; and it itemized our use of waterways as dumping grounds in a way that has generated severe toxicities in seafood such as methylmercury, PCBs, dioxins and heavy metals.
In Part III, there was a brief look at some of the alternative supplements for dietary essential fatty acids. Part IV addressed other dietary fats, the necessity of emotions in eating, the concept of behavioral eating and the fact that food is healing.
In Part V, the previous section, I laid out the history and use of body mass index and discussed how the human body is more capable of being short than tall and more fat than thin. And now let’s delve into the last four sections, where we really focus on our society’s misplaced fear and loathing of fat.
Obesity: Smoke and Mirrors
Very sheepishly I’ll admit it: despite years in “the business”, I accepted, without a second glance, that there was an “obesity epidemic”. That was until I read The Obesity Myth, by Paul Campos and subsequently got up to speed on Glenn Gaesser’s significant and solid body of research on the topic as well.
The facts are there is no obesity epidemic; obesity itself is not a killer; and it is not a health crisis that we are getting heavier, on average, in developed nations.
We cannot even dependably define what excess adiposity (fat stores) for a human being might be because if someone is optimally meant to be that way, then it cannot by definition be excess for that individual.
Certainly there is a point at which there is so much fat on a person that the fat impedes normal motion and the ability to get around. But that actually occurs at triple digit BMI levels only.
Let’s start with what obesity is generally assumed to be. It is supposed to be the accumulation of excessive body fat to the point where there may be, due to that excessive fat, an adverse affect on morbidity (illness) and/or mortality (earlier than average death).
According to the World Health Organization (WHO), the National Institutes of Health (NIH) and the Centers for Disease Control and Prevention (CDC) anyone over BMI 30 is obese and has an increased chance of Type II diabetes, sleep apnea, heart disease, stroke, osteoarthritis and endometrial, breast and colon cancers.
Anyone between BMI 25-30 is considered pre-obese.
There are two primary sources upon which the above health information, widely disseminated and generally presumed to be correct, was based:
- McGinnis, JM, Foege, WH. (1993) Actual causes of death in the United States. JAMA 270, 2207-2212.
- Allison, DB, Fontaine, KR, Manson, JE, et al.(1999) Annual deaths attributable to obesity in the United States. J Am Med Assoc 282, 1530-1538.
The first one did not even discuss obesity as a contributing factor for early death. In fact the authors of the study made attempts to try to stop having their data misrepresented [NEJM, 1999], but the data continue to be misinterpreted to this day.
In the second study the authors only controlled for age, sex and smoking and therefore assumed that if someone had died, and he or she was obese, that the only cause of death would have been obesity. A facile conclusion that neglects to control for levels of activity, genetic pre-dispositions to other serious illness, history of weight cycling, use and/or misuse of diet drugs, bariatric surgery…the list is long.
Overweight Means Eating Too Much
Statistics from the Healthy Eating Index [Table 10, 1998] show that adults with a body mass index of 20 or less and those with a BMI greater than 30 have similar calorie intakes, as do the two categories between.
Men (ages 18-74) who eat 60% of the recommended daily calories: 3% are BMI 15-20, 36% are BMI 20-25, 43% are BMI 25-30 and 17% are over BMI 30.
Men (ages 18-74) who eat 120% of the recommended daily calories: 3% are BMI 15-20, 46% are BMI 20-25, 41% are BMI 25-30, and 10% are over BMI 30.
Take a close look at that for a moment.
17% of those eating only 60% of the recommended calorie intake are obese. Only 10% of those eating 120% of the recommended calorie intake are obese.
The correlation coefficient is r=0.02594 (p<0.38), and that means that body mass index is not linked to calorie intake.
The next time someone you know decides to comment on a large person needing to stop eating so much, let them know she’s more likely to be eating too little.
Eating Fat Makes You Fat
The creation of fat stores appears to be more closely linked to excess carbohydrate ingestion and that lipogenesis occurs in situ (fat is created within the fat stores) rather than in the liver [A. Aarsland et al., 1997]. That does not mean that eating carbohydrates makes you fat, simply that dietary fat ingestion does not result in lipogenesis (fat store creation) in the same way as carbohydrate ingestion does.
Hypertriglyceridemia (high levels of triacylglycerol) is associated with an increased risk of cardiovascular disease. When subjects were placed on high-fat, low carbohydrate diets, triacylglycerol levels were not affected. With the low-fat, high carbohydrate diet, triacylglycerol levels increased significantly [J-M Schwartz et al., 2003].
Low-fat diets not only increase plasma triacylglycerol but also reduce HDL cholesterol levels (the good cholesterol) [S.E. Kasim-Karakas et al., 2000].
Therefore not only does eating fat not make you fat, but more importantly not eating fat increases markers that indicate risks for cardiovascular disease.
Disproportionate Fatness Increases Across Weight Categories
Over the past 25-30 years the average weight of human beings in most countries around the world has increased. But the increase is not the same across all weight categories.
Importantly not all of us are getting fatter at the same rate.
“While there has been significant weight gain among the heaviest individuals the vast majority of people in the ‘overweight’ and ‘obese’ categories are now at weight levels that are only slightly higher than those they or their predecessors were maintaining a generation ago. In other words we are seeing subtle shifts, rather than an alarming epidemic. Biologist Jeffery Friedman offers this analogy: ‘Imagine that the average IQ was 100 and that five percent of the population had an IQ of 140 and were considered to be geniuses. Now let's say that education improves and the average IQ increases to 107 and 10% of the population has an IQ of >140. You could present the data in two ways. You could say that average IQ is up seven points or you could say that because of improved education the number of geniuses has doubled. The whole obesity debate is equivalent to drawing conclusions about national education programmes by saying that the number of geniuses has doubled.’” [P. Campos et al., 2005].
Campos and his colleagues point out that within a generation, there has been no change to weights for those at the low end of the weight spectrum, a very modest increase of 3-5 kg. (8-17 lbs) for the majority in the average range of weights, and a much larger increase for those already at the heaviest ranges. [ibid.]
There is sufficient evidence that what has been nicknamed the “thrifty gene” may be responsible for why just under 5% of the population is now significantly heavier than 25 years ago. Aboriginal communities, in particular those who traditionally lived with long periods of severe privation, starvation and environmental hardship, favored those who could maintain low metabolic rates and store any excess energy available, are particularly prone to obesity over BMI 40 (class 3 obesity as it is known) in environments where food in now plentiful.
Please note that systematic review data is now available on this site regarding obesity correlates. Please review information under Papers.