What is the function of LDL? Fat?

In the previous chapter I reviewed how blood LDL is responsible for CHD and how statins lower blood LDL. If LDL is so detrimental to health, why does it exist? What purpose does it serve? In order to explain the role LDL plays in health, we need to step back and discuss fat, because in the end, LDL plays an important role in the transport of this important commodity throughout the body.

Fat, the body’s gasoline

The following slide shows the energy stores in a typical human. Each box represents a pool of stored energy and its approximate size (which can vary). On the right is the approximate daily kcal (2500 kcal) burned by a male. The carbohydrate stored in the body is just able to handle this daily energy need: liver glycogen (570 kcal) + muscle glycogen (2000 kcal) + blood glucose (38 kcal) = 2,608 kcal (total carbohydrate kcal available).   If you do not eat for 24 hours, theoretically all of this carbohydrate would be used up. Therefore, the body needs an additional energy depot – the fat.

Body Energy Stores

In reality, fat is used for energy during the day so that carbohydrate is not completely used up after 24 hours. For example, it is estimated that the heart, at all times, uses 95% fatty acids for it energy source. But the question remains, how do the fatty acids in the fat get to tissues like the heart? It turns out that the body has an intricate transport system that involves the lipoprotein families and the protein albumin, the jack of all trades.  And this transport system is very important, because if this system would fail for even a few minutes, the heart would run out of fuel and stop, and you would die. See the following figure.

Fatty acid Cycle

Adipose/Liver-Free Fatty Acid/VLDL cycle (for simplicity, aka “The Dixon” cycle)

Because the Dixon cycle is a cycle, it can start anywhere and end anywhere.  In the adipocyte (Fat cell), triglyceride (TAG) is broken down to free fatty acids, which then diffuse into blood and bind to albumin, the predominant protein in blood. Albumin carries (via Blood) the free fatty acids throughout the body – especially to muscle. The left over free fatty acids are taken up by liver, where they are re-synthesized into TAGs. Apolipoprotein B (ApoB) – a protein, wraps itself around (like a belt!) a triglyceride (TAG) and cholesterol lipid droplet to form Very Low Density Lipoprotein (VLDL). The liver hepatocyte secretes VLDL into the blood. VLDL permeates throughout the body and delivers fatty acids to tissues like heart, muscle, and bone marrow. An enzyme called Lipoprotein Lipase (LPL) is on the surface of the endothelium of blood vessels and “catches” the VLDL particles. Lipoprotein lipase reaches into the droplets and hydrolyzes the fatty acids off the TAG molecule. Eventually, the remaining fatty acids (in the form of TAG) in VLDL, are returned to tissues or adipose cells. In this way all of the tissues of the body have access to energy in the form of fatty acids (the body’s gasoline). In the final step about 50% of the VLDL that has been depleted of TAG are converted to Low Density Lipoprotein (LDL), which, after a half life of 3 days, is then taken up by the liver, using LDL receptors, in order to return the remaining cholesterol and other lipids to the liver.

The “Dixon cycle” can be speeded up in the following way: The more fatty acids that are released from adipose, the more fatty acids the liver needs to takes up, the more TAG is synthesized in liver, the more VLDL is secreted by liver.

Disturbances in parts of the “Dixon cycle” can be the cause of the following chronic problems:

1. Inability to mobilize fatty acids from adipose- poor exercise stamina because glucose is utilized too fast – normally fatty acids are used for low intensity exercise.

2. In obesity, too many fatty acids are released from adipose – more than can be used – and excess fatty acids need to be sucked up by the liver, which tries to quickly repackage them into TAGs and secrete them as VLDL. If the liver gets overwhelmed by excess TAG, a fatty liver develops.

3. Hypertriglyceridemia occurs when susceptible people eat very high carbohydrate diets – excess glucose is converted to fat in liver and increased synthesis of TAG causes increased VLDL secretion – the result is hypertriglyceridemia!

4. Lipoprotein Lipase deficiency – a person with this deficiency cannot even eat a moderate fat meal because blood triglycerides can reach enormous levels – into the 1000s mg/dL.

5. Abnormal body shape – fat in the wrong places, etc. – If lipoprotein lipase is in greater amounts in different areas of the body – fat is stored in these locations (see figure). This explains the different distributions of fat between men and women.  Depending upon the precise distribution of body fat, this may lead to an unhealthy metabolic situation, as what often occurs in men.  No matter what, most people I know are not happy with their their body shape! Now they know they should blame lipoprotein lipase!

6. Chronic overproduction of VLDL leads to increased production of LDL in blood if LDL receptor amount is low!!!  This condition leads to Combined Hyperlipidemia, the most common hyperlipidemia in humans.

Fatty Acid Cycling Male vs Female

Figure caption:  “Key sex differences in adipose tissue. Compared to men, women are characterized by increased amounts of brown adipose tissue BAT and enlarged peripheral fat depots, whereas intra-abdominal fat depots are preferentially increased in men. Sex differences in the metabolic and endocrine function of these depots are associated with diminished disease risk in women. FFA free fatty acids.”

KalypsoKarastergiou, Steven R Smith, Andrew S Greenberg and Susan K Fried. Sex differences in human adipose tissues – the biology of pear shape. Karastergiouet al. Biology of Sex Differences 2012, 3:13.



Fat is the body’s gasoline and must be available every second of every day.  Therefore, multi-tissue organisms have developed lipoproteins to transport lipids through the aqueous blood. Free fatty acids are released into the blood in excess and carried throughout the body on the protein, albumin.  Excess fatty acids are taken up by the liver, repackaged into triacylglycerol molecules (TAG), and send back through the body and returned to the adipose on VLDL particles. About half of the VLDL particles are converted to LDL, which is involved in returning spent VLDL particles back to the liver. LDL also delivers cholesterol to certain tissues that need a great deal of cholesterol, such as the adrenal glands, and tissues that are rapidly growing.   So the problems that humans encounter later in life with high LDL cholesterol in the blood are the result of disturbances in the complex fatty acid distribution system that is required to keep humans alive during the course of the day and any time that excess fat stores are needed as in during exercise or during starvation. Of course, we now have statins to help when LDL cholesterol is increased in the blood.  Additionally, pharmaceuticals are being developed to manipulate PCSK9 so that LDL cholesterol concentrations can be driven even lower!

What causes Coronary Heart Disease (CHD)?

The prevailing hypothesis right now is that CHD is caused by high levels of LDL over many years, although, as will be discussed later, other biological factors can either enhance the damage LDL causes or protect against excess LDL.

As I described earlier, LDL is a lipid droplet surrounded by a structural protein. The lipid droplet mainly carries cholesterol in the form of esters, and there are about 1500 cholesteryl ester molecules per LDL particle.

The most agreed upon mechanism how an increased blood LDL concentration causes coronary arteries to become blocked is that LDL invades the area under the the endothelial cell lining of the arteries (See following figure). This area, called the subendothelial space, becomes infiltrated with LDL particles and cells (monocytes/macrophages) that are charged with keeping the subendothelial space clean. In most of us, for much of the first 30-40 years of life, HDL particles return excess cholesterol to the liver for disposal and the plaque remains small and benign. But over decades, after the blood LDL cholesterol starts to increase, the process of cleaning out the subendothelial space can be overwhelmed, and cholesterol, debris, foam cells (engorged macrophages), and other constituents can accumulate in the artery wall and partially block the lumen (opening) of the artery.

Coronary Artery Diagram

A heart attack occurs when the artery is totally occluded. This occurs most often when a plaque from another region ruptures and travels to the site of the partial blockage and causes a total or near total blockage. When blood cannot flow to certain areas of the heart, heart muscle cells in that region do not get enough oxygen and die. This basic mechanism is extremely complex and involves many different cell types and a multitude of proteins and signaling molecules. The precise steps have still not been worked out and active research is still being conducted by many different laboratories.

The experimental evidence that LDL causes CHD was developed over a 50 – 60 year period after the discovery of the lipoprotein families and the development of methods used to isolate lipoproteins and study them and their metabolism.

Brown and Goldstein’s work with patients with familial hypercholesterolemia, some of whom died of heart attacks as early as six years old, showed that defects in the LDL receptor of cells were responsible for the very high build up of LDL in blood in most cases of patients with obviously some kind of hyperlipidemia.

What about the rest of us – those without a genetic hyperlipidemia? As also discussed earlier, the LDL receptor number or activity decreases with age. When combined with an atherogenic diet or with some other risk factor, the likelihood of developing CHD increases as we become older.

The Discovery of Statins

What to do about cholesterol and increased CHD in the rest of us was answered with a scientific discovery made by Akira Endo in Japan. Dr. Endo worked for Sankyo Chemicals and he was interested in finding an inhibitor of cholesterol synthesis in fungi, just as penicillin was discovered and isolated from the fungus, Penicillium notatum. After testing many different preparations from different fungi, Dr. Endo finally isolated a compound from Penicillium citrinum that could inhibit the enzyme HMG CoA reductase, an enzyme in the cholesterol synthesis pathway. After determining the structure of the compound, it was called mevastatin (also called compactin) due to its similarity to mevalonate, an intermediate in the pathway. Sankyo Chemical Company enticed Merck and Company in the US to become interested in mevastatin.

Using data and insights into mevastatin from Sankyo, scientists at Merck isolated, from a different fungus, a very similar compound that was a slightly more powerful inhibitor of cholesterol synthesis than mevastatin. This compound was call lovastatin, and it was approved by the Food and Drug Administration in 1987 and became the first prescription statin drug, known as Mevacor.

What Dr. Endo had discovered in the fungus was an active ingredient (mevastatin or compactin) that was capable of binding to and stopping the enzyme, HMG-CoA reductase, one of the early enzymes in the complicated pathway of cholesterol synthesis. The following figure gives clues to how mevastatin works. Mevastatin was extracted from the fungus and a portion of the molecule remarkably resembles the configuration of mevalonate, the intermediate in the cholesterol synthesis pathway. When mevastatin enters a cell, it binds to the enzyme that normally produces mevalonate from hydroxy methyl glutaryl Coenyme A. This prevents mevalonate from being formed in the reaction from the natural substrate. As you might expect, the tighter an inhibitor like mevastatin can bind to the enzyme, the more effective the inhibitor will be.

When studies noted that mevastatin could decrease LDL in the blood of humans, many pharmaceutical companied developed research programs to find compounds that were similar to mevastatin but more powerful than mevastatin. Therefore, as shown in the following figure, pharmaceutical companies developed a series of compounds that were very similar to mevastatin, but bound tighter to the HMG CoA reductase enzyme targeted in the pathway.

Different Statin Drugs

Thus, once the original chemical was isolated from the fungus, pharmaceutical company chemists worked to alter the structure slightly in order to improve the drug. This explains the rapid development of more potent statin drugs over the twenty year period after mevastatin was discovered in Dr. Endo’s fungal preparation. Several companies were indeed very successful and now this class of pharmaceuticals, known as statins, is one of the most prescribed drugs in the entire world.

But how do Statins Lower Blood LDL?

The mechanism how statin drugs lower LDL cholesterol, and thus total cholesterol in blood, is an interesting one. Although HMG CoAreductase is present in almost all cells, it is the enzyme in liver cells that is especially important for the regulation of blood LDL concentrations. As demonstrated in the following figure, after the statin binds to HMG-CoA reductase in liver cells, it inhibits the synthesis of cholesterol (Large cross bars in liver) in liver. Lower cholesterol levels in liver cells (Shown as a whole liver in the figure) are sensed and the cells increase the synthesis of LDL receptors, which go to the cell membrane.   The increased number of LDL receptors take up more LDL from blood so that the liver cells can have enough cholesterol for their membranes and other pathways.

Statins Increase LDL Recept in Liver

What have the Clinical Trials Told Us about Statins?

In 2010, a meta analysis of 21 trials involving statins vs placebo (129,526 individuals; median follow-up 4.8 years) and 5 additional studies that tested an aggressive statin dose versus a lower statin dose indicated that statins caused an all-cause mortality decrease of 10% per 1.0 mmol/L drop in LDL concentration (RR 0·90, 95% CI 0.87–0.93; p<0.0001). This decrease in mortality was largely due to decreases in coronary heart disease (RR 0·80, 99% CI 0.74–0.87; p<0.0001). Therefore, for every lowering of 1 mmol/L (39 mg /dl) of LDL cholesterol, a 10% reduction in CHD is expected. The large number of subjects put to rest the questions of whether statins increased deaths due to cancer or other non-vascular causes. The answer was that they did not.  Statins are fairly safe drugs, although side effects such as muscle pain are certainly a possibility.

Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Cholesterol Treatment Trialists’ (CTT) Collaboration. Lancet 2010; 376: 1670–81.


Why do some people not show increased blood cholesterol with an atherogenic diet or with increasing age?

The observation that some people are refractory to cholesterol has now been explained by the discovery of PCSK9, a protein that is involved in diverting LDL receptors for degradation inside cells (especially liver cells). When PCSK9 is mutated, individuals have more LDL receptors on their membranes. Approximately 1/30 persons have one allele coding for a mutation in the PCSK9 protein such that blood LDL cholesterol concentrations are decreased by about 15% and CHD is lowered about 45% in these people. In populations that have both PCSK9 alleles mutated, and thus have much higher LDL receptors on their cell membranes, LDL cholesterol was decreased by 40% and these lucky individuals presented with a 90% decrease in CHD. The presiding thoughts are that lifelong loss of PCSK9 protein leads to low blood LDL over a lifetime, very strong protection against LDL directed plaque development, and thus much lower rates of CHD. A small percentage of individuals have higher PCSK9 activity, and thus, they have higher LDL cholesterol levels and increased risk for CHD.

The PCSK9 story illustrates that the basic mechanism for removing LDL from the blood using the LDL receptor, as detailed by Goldstein and Brown, was correct, but that genetic diversity led to more complicated regulation than originally observed. The PCSK9 story also reinforces the role of LDL cholesterol levels in the basic etiology of CHD.

Many studies by investigators all over the world have given support to Ancel Keys’ original observation – that blood cholesterol, especially very high blood cholesterol concentrations, are associated with coronary heart disease, and in fact, as shown in later studies, LDL cholesterol was shown to be a direct player in increasing the development of coronary artery plaques. There is certainly evidence that other factors play a role in CHD, such that some people with high LDL do not get disease and some people with low LDL concentrations may develop disease. The differences in biological variability among people, even within fairly well defined and stable populations, are quite wide, such that making precise accurate predictions concerning which individuals will get CHD are difficult.

The three previous chapters covered three powerful changes in American society in the late 1900s that converged to overwhelm the energy regulation system in humans such that a large percentage of Americans became overweight or obese over a relatively short 30-40 year period.

To recap, these powerful forces were:

1.The development of a myriad group of food products that were both super palatable and energy dense, plus the proliferation of fast food restaurants, such that one was located at every highway exit and within walking distance of most Americans.

2.The infusion into the home of two powerful digital media systems that were able to hijack the spare time of most Americans leading to a sedentary life style.

3.The continued income inequality in the US coupled with a more dangerous neighborhood environment due to drugs, guns, and gangs compelled mothers and caregivers to keep their children inside watching television and appeasing them by feeding them absolutely addictive, nutrient poor, energy rich snack foods.

However, there are always forces within society that will take advantage of the complexity of an action and will propose an explanation that is simple, straight-forward, yet totally incorrect. I call these people, “the nutrition crazies” and they have written thousands of books shouting their view that one thing alone is responsible for the giant obesity earth quake that has changed the American landscape in such a drastic way.

One group of “the nutrition crazies” has blamed Ancel Keys and his discovery that high blood cholesterol was an important risk factor for CHD as a reason for the obesity crisis. Another group of “nutrition crazies” has blamed a shift to a greater percentage of total kcal coming from carbohydrate as the sole reason for our current obesity crisis. As in most philosophies put forth by quacks, there is some small element of correctness in their assertions that increased carbohydrate intake is an important factor in the obesity epidemic. But as we observed in chapter XI, there were increases in total kcal, carbohydrate, and fat intakes in the American population over this period of time, and all of these have contributed to the increase in obesity.

For the time being, lets discuss the carbohydrate versus fat argument.

When pure carbohydrate and pure fat are burned in a bomb calorimeter, the data observed is that carbohydrates contains 4 kcal/gram and fat contains 9 kcal/gram. The energy in these macronutrients is due to the bonds that are used in each molecule. This energy is derived from where each atom is bonded to its neighbor, and some bonds contain more energy than other bonds. It so happens that the sum of the bonds in 1 gram of fat contains more energy than the sum of bonds in 1 gram of carbohydrate. The basic energy in each of these macronutrients is determined by their chemistry and physics – not by magic. And in fact, these macronutrients have been used to store energy in cells since early evolution because each can do so in a relatively safe and efficient way.

The first law of thermodynamics in physics states that energy cannot be created or destroyed in a close system. Therefore, if these macronutrients are consumed by an animal, the inherent energy in them will not change. No matter what, the animal metabolizes these nutrients by biochemical reactions and the energy released when they are completely converted to their most simple products, carbon dioxide and water, must match the energy that was present in their original configuration. Therefore, the energy difference that was measured in the bomb calorimeter must be maintained in the animal system. This is basic physics and, in fact, this relationship was observed and confirmed many times in studies carried out in the late 1800s and early 1900’s. A review of this topic can be found in the excellent book, “The Fires of Life” by Max Kleiber, a scientist formerly at the University of California-Davis, considered the father of the field, Bioenergetics, which Is the study of energy conservation in living systems.

With the above said, there are situations where a metabolic situation can be established that favors energy storage rather then energy expenditure. However, in this situation, the equations explaining energy distribution must be upheld. The second law of thermodynamics holds in all living systems.

I will discuss this topic in greater detail in a later chapter. But right now I wish to return to the topic of cholesterol, because in the late 1900s discoveries were made that would have a great influence on our knowledge of lipid and cholesterol metabolism and that would lead to advances in medicine.


In a world full of ironies, a very sad yet interesting irony of our current obesity crisis is that poverty and food insecurity breeds obesity. It does this in several major ways.

1. Lack of funds to purchase nutritious foods and general food insecurity leads families to rely on nutrient poor, energy dense foods, especially during the last week of the food stamp cycle.

2. Obese girls grow up to be obese mothers, who give birth to very heavy babies, who are at increased risk for becoming obese children, and the cycle of obesity is set up to continue.

3. Mothers or care givers in poor neighborhoods prefer to keep their children safe by keeping them in the house or apartment rather then allowing them to play outside where they may be exposed to violence as a result of drug abuse and gang activities.   Since the children get bored staying inside watching television, mothers try to make their children content by buying them cheap, tasty, calorie dense snack foods.

Income Inequality is Real in the US

Income Inequality is real 2011 Atlantic Mag

1.Lack of funds to purchase nutritious foods and general food insecurity…..

Anderson (1990) stated that food insecurity occurs, “whenever the availability of nutritionally adequate and safe foods or the ability to acquire acceptable foods in socially acceptable ways is limited or uncertain.”

Anderson SA. Core indicators of nutritional state for difficult-to-sample populations. J Nutr. 1990;120:1559–1560

The USDA reported that in households with children, 17% experienced food insecurity without hunger while less than 1% experienced hunger in the children. In households without children, 8% experienced food insecurity without hunger and 4% reported hunger (USDA Economic Research Report # 11, 2004). The low amounts of hunger in households with children probably is a result of the WIC program, which supplements other aid programs when families have children.

Dinour and colleagues carried out a review of the effects of food insecurity on obesity in the literature published between 1996 and 2006. In their article they present and discuss each study that they considered large enough and that included well described methods. They found a relationship between food insecurity and body weight in women but not in men. This makes sense as men spend a large amount of time out of the home.

Dinour and co-authors also found no association between children being overweight and food insecurity. This last observation is also thought to be the result of extra nutrition provided by the WIC program and because mothers and caregivers often protect their children by giving them available food. However, an important wrinkle to this relationship occurs if the mothers are obese, as will be discussed directly below.

Dinour LM, Bergen D, Yeh MC; The food insecurity-obesity paradox: a review of the literature and the role food stamps may play. J Am Diet Assoc. 2007 Nov;107(11):1952-61.


2.Obese girls grow up to be obese mothers….

An explanation for obesity that applies specifically to infants and very young children is that, now that we have been in the obesity epidemic for at least 20 – 25 years, obese mothers are now giving birth to very large babies that have a high probability of growing up obese. In fact, an article by Gorman’s group (see below) indicated that, in the 28,000 children (2 to 5 years old) in the Massachusetts WIC program, the strongest association with obesity observed was the birth weight of the infant.

The conclusions of this study were:

“The results of this study point to a significant association between persistent household food insecurity without hunger, young children’s weight status, and risk of childhood obesity. It is noteworthy, however, that the associations depend on maternal weight status. Given that results imply that specific groups of children are particularly vulnerable to adverse effects of household food insecurity, targeting these groups might be necessary.”

But this study was amazing in another straight-forward way.  And that was the fact that there were, in the first place, 28000 children who qualified for WIC in Massachusetts alone. This is absolutely amazing to me. How is it that in a highly developed country there can be 28000 children who require nutrition assistance in only one of fifty states?

Metallinos-Katsaras E, Must A, Gorman K. A longitudinal study of food insecurity on obesity in preschool children.
J Acad Nutr Diet. 2012 Dec;112(12):1949-58.


(You will need to obtain the full article through Rutgers Libraries)

3.Mothers or care givers in poor neighborhoods prefer to keep their children safe….

……by keeping them in the house or apartment rather then allowing them to play outside where they may be exposed to violence as a result of drug abuse and gang activities.   Since the children get bored staying inside watching television, mothers try to make their children content by buying them cheap, tasty, calorie dense snack foods.

The above was presented to my Obesity class in a lecture by Dr. Debra Palmer.

The Fight Against Obesity is Carried out by Amazing, Awe-inspiring Individuals

Dr. Palmer is an amazing health professional whose life’s work is to help lower income people have better health through improved nutrition. But even more interesting is Dr. Palmer’s own life story and educational path to become a Professor at Rutgers University.

Dr. Debra Palmer grew up in the inner city of Cincinnati, Ohio. She realized that she needed to go to college in order to break out of the cycle of poverty and, as a single mother, to give her son a better life and insurance (he was asthmatic).  Dr. Palmer went to college for aerospace engineering. During this time she needed food stamps to supplement her and her son’s diets. After obtaining her undergraduate degree, Debra taught physics and chemistry in high school in inner city schools. During this time, Dr. Palmer came to the conclusion that most inner city children had no idea how to successfully navigate modern society and she decided to change her educational goals to specifically help the children of the inner city.

Dr. Palmer obtained 2 Master degrees, one in Education and the other in Nutrition. And later she went on to obtain a Ph.D. degree in Nutrition from Penn State University. During her Ph.D. studies, Dr. Palmer became familiar with government programs that were designed to help prevent hunger in the poor. One of them was Supplemental Nutrition Assistance Program – Education (SNAP-Ed, this was the education portion of the program formerly known as the food stamp nutrition education program (FSNE)). The other program was the Expanded Food and Nutrition Education Program (EFNEP). This program was specifically designed to help provide nutrition education to families with children.

After Dr. Palmer graduated with her Ph.D. and moved to New Jersey for a faculty position in Nutrition, she set about using her knowledge to bring SNAP-Ed to New Jersey, and to make these government educations programs efficient and helpful to the populations in New Jersey they were meant to serve. Having grown up in the inner city and having received food stamps while she was in college, Dr. Palmer was aware of the special problems that face poor people in urban areas.

Her strategy included three major operational tracts:
1) She studied the Federal laws so that the State of New Jersey could obtain the maximal amount of funds for nutrition education from the different legislation bills passed by Congress.

2) Dr. Palmer used her knowledge of the difficulties of urban city living to develop effective educational tools and plans. This has even progressed to the the production of educational videos that promote healthy practices, such as exercising at home. See http://www.snaped4me.org

3) Finally, Dr. Palmer hired and trained an army of people from the different communities all over the state (people with high school diplomas (but not bachelor degrees)) and trained them to teach in the community, and along the way, to become successful Rutgers University employees, who were eligible to take college classes in order to work toward college degrees. Over the last 10 years she estimates she has obtained a 66% success rate in hiring competent and loyal community workers for her programs.

Income Inequality Certainly Involves the Physical Environment that Poor People Live In

The Physical Environment is defined as our current structured environment where people (adults and children) live, eat, play, shop, work, and attend school. Therefore, the Physical Environment includes the Neighborhood food environment, Neighborhood parks and playgrounds, Neighborhood walkability, Neighborhood public transportation, and Neighborhood safety. The Physical Environment, in most cases, cannot be altered unless the individual and family move to a new location.

In a review of studies by Booth and co-authors (2005), there was strong evidence that:  “…….research presented in this review clearly demonstrate strong preliminary evidence of a relationship between built environment features and the prevalence of obesity. Lower SES neighborhoods are a primary concern, as residents in these areas may have less access to recreational facilities or food stores with healthful, affordable options, …….”

Booth KM, Pinkston MM, Poston WS. Obesity and the Built Environment;  J Am Diet Assoc. 2005;105:S110-S117.


The impact of safe playgrounds on obesity was studied by Dr. Yanjong Jin of Rutgers University (2013).  Dr. Jin used the 2007 National Survey of Children’s Health (NSCH) to determine what effects the presence of a neighborhood park had on the obesity rate of children. Dr. Jin and her co-author found that the effects of a park/playground on childhood obesity was dependent upon the gender, age, race, household income level, neighborhood safety, and other neighborhood amenities. Of high importance was the safety of the neighborhood.

The following received more benefit from a safe neighborhood park:

1. The benefit was greater in girls than boys

2. The benefit was greater in the age 10 – 13 group

3. Non-Hispanic white youth benefited more than other groups

4. Children in unsafe neighborhoods benefited more

The take home message from Dr. Jin’s study was that we need to consider the environment people live in when strategies to combat the obesity epidemic are developed. However, if mothers are afraid to allow their children to play outside, it doesn’t matter what physical environment is available outside their houses.

Maoyong Fan and Yanhong Jin; Do Neighborhood Parks and Playgrounds Reduce Childhood Obesity? Am. J. Agr. Econ. (2013) doi: 10.1093/ajae/aat047 First published online: August 6, 2013

Published article can be found at:



In the previous chapter I documented changes that occurred in food intake in the period after 1970. If that was all that occurred, it is possible that the energy regulation system in most individuals could have withstood the powerful forces that they faced concerning super palatable foods.

But in addition to the major changes that occurred in the availability of kcal in myriad foods and the explosion in fast food restaurants, another major earth quake was taking place in American society.

At the exact same time that there were major changes in food supply and consumption, there occurred many changes in the ways Americans accessed media – all due to the advances in transistor based technologies.

The graph below shows the history of TV over its first 75 years. By about 1960, over 90% of households contained a black and white TV.   By 1980, over 80% of households contained a color TV and about 50% of households held more than one TV. But starting at about 1980, additional changes occurred in American households concerning television viewing. At about 1980, the percent of houses wired with cable television was only 20%, but by the year 2000, this percent increased to 70%. Also about 1980, remote controls and video cassette recorders (VCRs) started to appear in homes. By 1990, already 70- 80% of households contained remote controls and VCRs. In a 10 year period starting in 1980, the way Americans watched and utilized televisions and related equipment became much more sophisticated and diverse.

TVs and Equipment in Am homes

The VCR data is especially interesting and relevant to me because one of my favorite stories from when my son (born in 1988) was small was that he developed an English accent because he had watched the film, Mary Popins, so many times. He also watched TV, but he especially liked to watch “Disney” movies that were becoming available on video cassette. The data on wired cable television shows that households began to receive many more stations than the locally available broadcast networks provided. The VCR and cable data accentuates the concept that the role of television in the home includes much more than just watching network programming. Also, viewing sporting events became much easier as sports only programming appeared. For example, ESPN was launched in September 1979 and has steadily increased in popularity. Since the birth of ESPN, sports only networks have proliferated on cable television.

By 2007 the average American home received 119 channels including 17 broadcast TV stations (Nielsen).


There is quite a substantial literature concerning the effects of watching television on the activity levels of children and adults. I will refer to some of these studies below. But just observing how television and all of its connecting media suddenly expanded in complexity leads to the straightforward hypothesis that physical activity was strongly curtailed by all the extra time spent watching media in the home.

If this was all that happened during this time period, Americans maybe could have adapted to the lower activity levels that accompanied the explosion in television viewing. But another very large technological advance occurred at this time that would have great effects on both home life and work in the office.

Computers in our lives

When I was writing my Ph.D. thesis in 1982, I would write in the library using paper and pencil during the day and later type what I had written using a typewriter at night when it was quiet in the lab. A colleague from my lab was also writing his Ph.D. thesis at the same time. However, he was using a desk top computer that had just become available in Madison, Wisconsin. The computer he was using was the Apple IIe. I was jealous of him but there was nothing I could do because there were no other similar computers in our entire building. Interestingly, we both completed our writing in late fall 1982. Therefore, I remember quite vividly when desk top computers became routinely available for practical writing purposes.

In the figure below the production and shipping of desk top computers is shown from their introduction to 2011.

Computers shipped - diff kinds

The figure shows by 1995 a little under 50 million computers were being shipped per year. Again I have a personal recollection of this time as my 5-year old daughter (born in 1991) had mastered all of the computer game programs that were available for the Macintosh computer in our local library. The library owned fifteen different programs for children and my daughter could sit in front of the computer for several hours without lifting her head. Before my eyes I was seeing the amazing mesmerizing capabilities of the desk top computer. Therefore, by approximately 1995, there were fairly sophisticated games that could be played by children for hours and hours. I was there and personally observed it!

The figure below breaks up the different kinds of computers that were made during this period. The data plotted in this graph shows the introduction of computers during the first years of the personal computer.

Computers shipped per year w author

The figures below show the times that were spent watching television versus surfacing the Internet by computer in the English adult population in 2006. The data, collected by IBM, show that respondents used the Internet more hours per day than they watched television. The researchers suggested that part of the reason for this observation were the extra hours used to surf the Internet during personal time at work.

Daily Internet UseDaily television viewing

There are many studies that describe the effects of the increasing use of electronic media on physical activity and health. The above figures show that the influx of all the possible ways to spend time using electronic media led to a convergence of effects such that we have been transformed to a largely sedentary society.

Tremblay and colleagues performed a systematic analysis of 232 studies with almost 1 million children. The authors concluded,

“Qualitative analysis of all studies revealed a dose-response relation between increased sedentary behaviour and unfavourable health outcomes. Watching TV for more than 2 hours per day was associated with unfavourable body composition, decreased fitness, lowered scores for self-esteem and pro-social behaviour and decreased academic achievement.”

In the same article the authors related that Intervention studies showed that many of the above negative effects were reversed when children spent less than 2 hours per day viewing television.

Mark S Tremblay, Allana G LeBlanc, Michelle E Kho, Travis J Saunders, Richard Larouche, Rachel C Colley, Gary Goldfield and Sarah Connor Gorber. Systematic review of sedentary behaviour and health indicators in school-aged children and youth.

Online open access:   http://www.ijbnpa.org/content/8/1/98

Increased television availability not only decreased daily physical activity, but it also affected sleep was in children. The presence of television sets in the bedrooms of children was observed to significantly shorten their nightly sleep time (2014).

Elizabeth M. Cespedes, Matthew W. Gillman, Ken Kleinman, Sheryl L. Rifas-Shiman, Susan Redline and Elsie M. Taveras.  Television Viewing, Bedroom Television, and Sleep Duration From Infancy to Mid-Childhood; Pediatrics 2014;133: e1163–e1171


Convergence of Use of Digital Media on Sedentary Behavior in the US

The Centers for Disease Control (CDC) collects yearly data concerning inactivity throughout the United States. The CDC data are remarkable, and one can easily go to the CDC website in order to view PowerPoints that show the year by year increases in inactivity, as well as the increases in the obesity rates and the increases in the number of diagnosed cases of Type 2 Diabetes.

Website: http://www.CDC.gov/diabetes

I was amazed how the maps for the different parameters had similar distributions showing the areas of high incidence of inactivity and disease throughout the US. On the next slide, I placed the distribution maps for inactivity, obesity, and diabetes on the same slide. The similar distributions are eye opening!

Maps of Inactivity, Obesity, and Diabetes in the US 2008

In the following slide, seven regions with extremely high inactivity are demarcated:

Maps of Inactivity, Obesity, Diabetes with selected areas

Close up of Inactivity Map:

Close-up of Inactivity Map

The seven areas indicated on the map are summarized here:

1.The states of Louisiana, Mississippi, Alabama, Tennessee, Kentucky, and West Virginia have high rates of inactivity, obesity, and Type 2 diabetes.

2.Eastern Kentucky and most of West Virginia have extremely high rates of inactivity and obesity (See map close ups bellow).

3.Eastern Oklahoma has a dense area of inactivity, obesity, and diabetes.

4.There is narrow strip in western Arizona and southern Utah that represents the location of various Native American tribes that have high rates of inactivity, obesity, and diabetes.

5.Northern Maine has a region of overlapping high rates of inactivity, obesity, and diabetes.

6.There is a elongated region of central California that represents the central valley that has overlapping high rates of inactivity, obesity, and diabetes.  There is much less inactivity along the coast.

7.The one bright spot in the country is Colorado, where there are light areas for all the parameters, thus relatively lower rates of of inactivity, obesity, and diabetes, compared to all other regions of the US.

The maps (from 2008) depict extremely strong data that point convincingly to the role of inactivity in the obesity epidemic.  Why are these areas especially prone to inactivity and obesity?  The answers are complex and differ from state to state and area to area.  Obesity is also the result of other factors such as healthy food deserts and an obesogenic built environment.  Some of the possible non-nutrition reasons for the high rates of low inactivity are listed below:

1.High inactivity in areas of the deep South may be due to high summer temperatures and humidity, forcing people to stay indoors in air conditioning.

2.High summer temperatures and humidity may be the reason for high inactivity in Eastern Oklahoma and Eastern Kentucky and most of West Virginia, too.

3.Northern Maine may have the opposite situation where the very long, cold winters keep people inside.

4.The narrow strip in eastern Arizona is populated by native American tribes that live on reservations that are located in areas with extremely high summer temperatures.  In addition, it is well known that Native Americans have “thrifty” metabolism that leave them susceptible to obesity on a “western type diet.”

5.The State of Colorado is a region of higher relative activity and, therefore, is somewhat resistant to the increase in obesity found in other areas of the US.


It is true that all of the data presented in this chapter consist of associations.

But starting in the the 1970s and 1980s very large eruptions occurred in our society that led a large percentage of individuals, especially children, to change such that our country went from a population that performed moderate physical activity to a population that was largely immovable and sedentary.

The unmistakable conclusion that can be extracted from all the data that were presented in this chapter is that a significant portion of the increase in obesity, starting in about 1970, was the result of waves of advances in digital media and the adoption of these in every aspect of life. Of especial importance was the introductions of cable TV, VCRs, and the remote control device, which collectively led to more sophisticated media viewing. Then barely fifteen years later, the infusion of desktop computers, such that by the year 2000, most households had both sophisticated television systems and easy to use desk top computers available for attention addiction. The introduction of each of these two major digital systems caused a powerful assault on the biology of the human, such that the energy regulation system that was developed over millions of years of evolution was completely overloaded within a short 20-30 year period.

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