In this article, I suggest {1} that "obesity" {2} is a group of independent diseases that are caused by separate pathological pathways. I also suggest that the independent pathways to these pathologies originated in the eruption, after 1945, of the second stage of industrialization of the food supply, based around synthetic foods, and the industrialization of medical care, based around antibiotics and synthesized pharmaceuticals.
Tracing the origins of obesity in any society, you are led back to the industrialization of its food, the mass treatment of many diseases by antibiotics and synthesized pharmaceutical medicines, and the collapse of the natural inclination to strengthen one's body, mind, and health by bodily exercise.
The historical changes in food and medicine are connected by auto-immune diseases and inflammation. Industrialized foods generate chronic inflammation and, through chronic inflammation, auto-immune diseases. Contemporary medicine's antibiotic strategy reinforces these problems by destroying the natural bacterial balance in the human intestinal tract from mouth to colon. The resulting pathological states cause weight gain as a distinct and necessary stage in the etiology of obesity, which, assaulted by chronic inflammation, leads to obesity.
As I will discuss in the next article, the medical literature also hints that these pathologies and their pharmaceutical medical treatments create, as another side effect, lethargy and "laziness". Sub-clinical, pathological demotivation to exercise removes a major natural treatment for weight gain, thereby reinforcing the tendency toward obesity.
While public health researchers believe that obesity is a single disease and caused by disruption of the caloric balance (a conception to which I object in the first article in this series), they nonetheless admit that multiple "contributing factors" are involved in the rise of obesity. The CDC lists as contributing factors: genetics (1), diet, metabolism, lifestyle, socio-economic status, custom, and disease and drugs. (See also Wikipedia.) Examine these "contributing factors" carefully and you will see that the CDC is actually talking about etiological routes to pathologies.
The following, six innovations in the post-1945 food supply and medicine are widely regarded as dramatic departures from historical patterns:
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Increased sugar content (refined sugars, high fructose corn syrup, and fruit sugars) in industrially processed foods and beverages;
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Increased saturated fat content in industrially processed food and beverages;
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Indirect introduction of synthetic hormones into the general food supply;
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Indirect introduction of synthetic pesticides and other toxins into the general food supply;
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Mass use of synthetic steroids and presciption medicines in medical care;
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General adoption of antibiotic prescription medicines.
In addition, other developments have raised researchers' suspicions of connections to obesity, but the scientific evidence of the connections is inconclusive. These developments include the pasteurization of liquid milk and other dairy products and feeding infants commercial formulas rather than mother's breast milk.
Let's take up the six, major developments, one by one.
(1) Refined sugars, including high fructose corn syrup, in industrially processed foods cause chronic inflammation.
The food industry maintains that the effect of HFCS is not clinically distinguished from cane sugar, 1. However, fructose has a different metabolic pathway than sucrose and does not lead to the release of leptin. Without the release of leptin, the consumer does not get the feeling of fullness that motivates him or her to reduce consumption. As a result, HFCS is over-consumed, dramatically increasing the caloric intake, while the consumer's health conscience, so to speak, is napping. This effect strengthens the statistical relationship between the use of HFCS in food processing and the rise of obesity since 1970.2
- Sugars cause inflammation (1, 2)
- Inflammation, not obesity, causes diabetes II (1, 2, 3)
- Obesity reinforces the effect of sugar by causing inflammation too (1)
- Sugars cause insulin resistance which leads to inflammation (1, 2)
Sugar has another effect. In processed foods, it masks food sensitivities (food intolerance) in the consumer. Sugar brings such gustatory pleasures that divert the consumer from realizing that foods to which s/he is intolerant are creating low grade, chronic intestinal inflammation. Food sensitivities can produce secondary inflammation, such as asthma.(1, 2) Food sensitivities also generate weight gain (1).
(2) Some saturated fats cause inflammation. They increase the level of inflammation markers in the blood. They decrease the ability of insulin to control blood glucose levels, therefore causing a pre-diabetic syndrome (1). They decrease the ability of HDL to protect the vascular system from inflammation, thereby increasing the rise of heart disease (1).
(3) (5) Steroids and many prescription medicines cause weight gain. Prednisone, an anti-inflammatory steroid hormone, is notorious for causing weight gain. Anti-depressants and other mood disorder medications also discourage their users for the side-effect of weight gain. Other controlled drugs that cause weight gain include ones for diabetes, blood pressure, seizures, and migraines. Their weight gain is usually beyond willful moderation by the patient (this testimony is typical). Some medicines can cause ten pounds of weight gain a month (1, 2). (There is no link between birth control pills and weight gain.)
(4) Pesticides and other toxins ingested with food produce inflammation. (1, 2);
(6) To treat these inflammatory pathologies, physicians prescribe steroids, anti-inflammatory medicines, and antibiotics.
The wide application of antibiotics destroys the helpful and benign bacteria species, which keep in check harmful bacterial species in the human gut. Harmful bacteria multiply, causing inflammation in the intestines and other organs of the body as the immune system attempts to halt their advance. Intestinal Inflammation becomes a chronic, pathological state. (The Wikipedia article on gut flora is useful on this subject. Also, 1, 2)
There are other bodily mechanisms involved in creating inflammation, especially insulin production and regulation of sugar levels in the blood, related to diabetes; the histamine reaction that fights antigens, related to allergies; the immune reaction that leads to rheumatoid arthritis; and effects of chronically inflamed blood vessels can trigger heart attacks.
How does chronic inflammation cause obesity?
When the body is chronically inflamed, the inflammation reaches all organs of the body; it is systemic. Every body, even the most lean person, contains fat cells (adipose tissue), which also become inflamed. The immune system pumps special killer cells into the fat cells to destroy disease agents. These immune system cells release chemicals that further increase inflammation. Normally, in acute but not chronic inflammation, removal of the provocative agent would allow other chemicals to signal the immune system to withdraw its attack in the afflicted cells. However, in the case of chronic inflammation, which is caused by a continual state of provocation, such as by excessive sugar in the blood, the chemical agents that shut off inflammation and signal the immune system to withdraw are never released.
Two major bio-chemical results of the inflammatory attack on the fat cells are insulin resistance (1) and leptin resistance (1, 2).
Update. December 5, 2009. Science, the magazine of the AAAS, reviews the state of research about and understanding of insulin resistance and its relation to obesity. Gary Taubes, "Prosperity's Plague," Science, vol. 325, 17 July 2009, p. 256 ff. (1)
The effect of inflammation on fat cells goes through two stages. The first stage is non-obese weight gain, which, adapting a medical diagnostic term (1), I call metabolic syndrome weight-gain. In this stage, moderate exercise can over-come both insulin and leptin resistances (1, 2, 3). The stage of non-obese weight gain is crucial, because the effect of inflammation on the fat cells causes chemical and genetically-linked chemical changes that push weight gain up to obesity. Obesity is a second stage. In this stage, exercise and diet lose their effectiveness in controlling weight-gain. Insulin resistance and leptin resistance are unchecked. (1, 2, 3, 4)
The Kinds of Obesity
The collection of symptoms, extreme overweight, high blood pressure, lethargy, inability to control appetite, no more indicates a single disease than having a runny, stuffy nose, watery eyes, sore throat, coughing, and feeling tired indicates a single disease. That stuffy nose and sore throat could be a cold or it could the flu. Similarly "obesity" could be medical obesity, caused by prescription medicines, or a consequence of an industrial diet with excess sugar and saturated fats, or some other cause.
The pathways of the different kinds of obesity have different origins, different stages, different rates of progression, and involve different bio-chemistries. I am not a medical or scientific researcher in any of the fields required to begin a technical redefinition of the taxonomy of pathologies of obesity and its precursor states; but I am confident, from a reading and synthesis of popular and semi-technical literature on the subject, that eventually medicine will distinguish between and bring different therapies to the different kinds of obesity.
The Perfect Storm
I refer to the increasing incidence of obesity as a perfect storm, because food and medical developments, that were originally believed to have no relationship, came together to create a group of diseases that resulted in obesity. Taken singly, each development would not be powerful enough to have generated the eruption of obesity; coming together, they did.
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Useful web sites.
On obesity: adipocyte, American Diabetes Association, CDC
On inflammation: PCOS
Wikipedia on: adipose tissue, diabetes, gut flora, inflammation, insulin resistance, leptin resistance, obesity
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Notes.
{1} I understand that my suggestion does not rise to the level of a hypothesis. I am not professionally competent in the scientific and medical fields needed to frame my ideas as a hypothesis. I simply draw upon publicly available medical popularization to provide a different view of the obesity phenomenon.
{2} I place the term, obesity, in quotation marks to indicate that it should no longer be considered as referring to a single, unitary medical condition.
Revised. January 21, 2009, February 17, 2009, April 29, 2009.
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The Causes of Obesity
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