Fat: Part Six
No More Fear No More Contempt
As a refresher for the series so far, Part One 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 Two, 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 Two 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 Three there was a brief look at some of the alternative supplements for dietary essential fatty acids. Part Four addressed other dietary fats, the necessity of emotions in eating, the concept of behavioral eating and the fact that food is healing.
In Part Four, 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; fatness itself is not a killer; and it is not a health crisis that we are getting heavier, on average, in developed nations [ed. update 2024 and have no subsequently evened out and are no longer getting heavier in the past two decades].
We cannot even dependably define what excess adiposity (fat) 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 may impede normal motion and the ability to get around. But that actually occurs at triple digit BMI levels only and is exceedingly rare.
The “Evidence”
Let’s start with what being fat 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 what they term “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 they consider 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 fatness as a contributing factor for early death. In fact the authors of the study made attempts to try to stop having their data misrepresented, but the data continue to be misinterpreted to this day. [1]
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 BMI≥30, that the only cause of death would have been that BMI. 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
Nope.
Statistics from the Healthy Eating Index [2] 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 BMI>30. Only 10% of those eating 120% of the recommended calorie intake are BMI>30.
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 they’re more likely to be eating too little.
Eating Fat Makes You Fat
Nope.
The creation of fat 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. [3] That does not mean that eating carbohydrates makes you fat, simply that dietary fat ingestion does not result in lipogenesis (fat 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. [4]
Low-fat diets not only increase plasma triacylglycerol but also reduce HDL cholesterol levels (the good cholesterol). [5]
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. [ed. update 2024, since 2000 average weight has remained flat in most developed nations around the world]
Importantly not all of us were 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”
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. [7]
There is fairly solid 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 starvation and environmental hardship, favoured those who could maintain low metabolic rates. These groups are particularly prone to BMI>40 (class 3 obesity as it is known) in environments where food in now plentiful.
Please note that more recent detailed reviews are also available now on EDI: Weight Gain Correlates in Literature.
Lyons P. Prescription for harm. The fat studies reader. 2009 Nov 4:75-87. p. xvi
Variyam JN, Blaylock JR, Smallwood DM, Basiotis PP. USDA's Healthy Eating Index and nutrition information.
Aarsland A, Chinkes D, Wolfe RR. Hepatic and whole-body fat synthesis in humans during carbohydrate overfeeding. The American journal of clinical nutrition. 1997 Jun 1;65(6):1774-82.
Schwarz JM, Linfoot P, Dare D, Aghajanian K. Hepatic de novo lipogenesis in normoinsulinemic and hyperinsulinemic subjects consuming high-fat, low-carbohydrate and low-fat, high-carbohydrate isoenergetic diets. The American journal of clinical nutrition. 2003 Jan 1;77(1):43-50.
Kasim-Karakas SE, Almario RU, Mueller WM, Peerson J. Changes in plasma lipoproteins during low-fat, high-carbohydrate diets: effects of energy intake. The American journal of clinical nutrition. 2000 Jun 1;71(6):1439-47.
Campos PF. The obesity myth: Why America's obsession with weight is hazardous to your health. Penguin; 2004.
ibid.
