“Hi, boss, I can’t come to work today. The inversion was so bad yesterday, that I woke up this morning with my butt too big, so I have nothing to wear.”
“Hi, boss, I can’t come to work today. I caught a cold yesterday, I woke up this morning with a huge derrière; plus, I don’t want to infect my co-workers.”
Ludicrous! Bosses have heard every excuse imaginable for not coming to work, especially on fresh powder days. The two excuses above are ridiculous, I know, but I wouldn’t rule out the possibility of a creative, alpine-addicted worker trying them in the not-too-distant future, when the significance of the articles highlighted below hits the popular media.
The first article, for the first excuse, is rather shocking. Its implications cut across virtually all specialties. As the Chairman of the UMA Environmental/Public Health committee, I feel it is my responsibility to share it with you. You may feel the article may be open to interpretation, so I will present it to you in bullet points, and quote its devastating implications:
“Persistent pollutants and the burden of Diabetes,” (J. Lancet 2006;368:558)
- Dioxins, polychlorinated biphenyls, dichlorophenyldichloroethylene from DDT/DDE, trans-nonachlor, hexachlorobenzene, hexachlorociclohexanes, plus many other chemicals, like phthalates for plastics are commonly found in humans (“The chemicals within us,” National Geographic, October 2006, p. 116).
- A study analyzed these persistent organic solvents and fasting plasma glucose concentrations in a random sample of a general population, from 1999-2002 (“A strong dose-response relation between serum concentrations of persistent organic pollutants and diabetes …” J. Diabetes Care 2996;29:1638).
- The prevalence of Diabetes was five times higher in groups with higher concentrations of these toxins. The prevalence of diabetes doubled and tripled in the upper quintiles of DDE and other compounds.
- The body burden of these fat-soluble chemicals often increases with increasing body-mass index. This means that fat stores more toxins.
- Might diabetes cause a higher accumulation of persistent organic pollutants?
“People with diabetes would be more likely to experience the adverse effects of these pollutants” (J. Environmental Health Perspectives 2001;109:871). - “There was no association between obesity and diabetes in individuals with non-detectable levels of toxins. Obesity was a risk factor for diabetes only if people had blood concentrations of the pollutants above a certain level. This finding might imply that virtually all the risk of diabetes conferred by obesity is attributable to persistent organic pollutants, and that obesity is only a vehicle for such chemicals. This possibility is shocking.”
- Michigan study associated diabetes with PCBs: People with higher PCBs had double the incidence of diabetes (J. Epidemiology 2006;17:352).
- “The causal role of toxins in diabetes is more likely to be contributory and indirect, i.e., through immunosuppressant, non-genotoxic, perhaps epigenetic mechanisms.”
This is a shocking report, indeed. It is too bad the conclusion ignores cutting-edge research showing that the main problems with diseases are metabolomic/energy issues, due to poor cell communication of information, as we see operating in the entire universe (Programming the Universe, Seth Lloyd; Knopf Press, 2006). Cell membranes are losing their ability to communicate, thus diminishing the energy cells need to do their job. Due to toxins, bad food and emotional stress our cell membranes are “TOIL-ing:” T = Toxic,
O = Oxidized,
I = Inflamed,
L = Lacking in energy (JAMA 2004;291:358).
A TOILing terrain explains insulin resistance and practically all chronic diseases. Also, the authors don’t discuss the concept that cell membrane dysfunction triggering insulin resistance is likely going to lead to many other problems, or resistance to other cell messengers. Thus, we get resistance to neurotransmitters, other hormones and immune messengers. Sure enough, these toxins have also been associated with cancer, neurological problems (J. Lancet 2006;368:2167) and many hormonal problems, especially thyroid and adrenal dysfunction.
And now let’s discuss the other far-fetched excuse. Again, here is the bulleted evidence:
“Obesity and gut flora,” J. Nature, December 21st, 2006;444:1009
- Flora in intestines influence how we metabolize and manage the food we ingest.
- Transplanted gut bugs from obese mice to lean mice cause the thin animals to get fat.
- Food additives, antibiotics, or other factors cause a fundamental shift in gut flora, making it easier for many people to gain weight.
- The gut flora from 12 obese people was compared to that of lean people. The obese had more organisms called firmicutes than bacteroidetes. As they lost weight, the proportion of firmicutes fell and bacteroidetes rose. Firmicutes are better at extracting calories from food.
The concepts above have already been covered by the lay press: (“Fat factors,” New York Times Magazine, August 13, 2006, p 28)
- Pennington Biomedical Research Center in Louisiana: Dept. of viruses and obesity, and Microbiologists at Washington U. in St Louis are looking for trillions of microbes in intestines contributing to obesity.
- Intestinal microflora extract calories from the food we eat, and help store them in fat cells: “infectobesity.”
- By the age of two, microflora is established in people. Modest differences in microflora may make big difference in metabolism.
- Intestinal flora has 78 million base pairs, or genes, and perhaps the number is 100 times that. Most genes a human carries are microbial: “Humans are super-organisms whose metabolism represents an amalgamation of microbial and human attributes.” Human + microbial genes = metagenome.
- Sterile mice without intestinal organisms had 60 percent less fat than ordinary mice, even thought they ate 30 percent more food. When these mice were given intestinal flora from ordinary mice, they gained weight and stored fat.
- Gut bacteria (B. theta) suppress protein FIAF, which prevents body from storing fat. M. smithii interacts with B. theta to extract additional calories from polysaccharides in diet. Humans colonized with these bacteria have 13 percent more body fat.
- Normal weight mice have more bacteroidetes than firmicutes. Obese mice have 50 percent less bacteroidetes, and 50 percent more firmicutes
- Meaning: cereal box says 100 calories per serving, but not every one will get the same amount of calories from the cereal. So much for the “calories in = calories out” dogma (American J. Clinical Nutrition 2007;85:346.)
- Chicken infected with SMAM-1 adenovirus have enlarged livers and kidneys, atrophied thymuses and excess fat in the abdomen. The study infected chicken with SMAM-1, which became obese. They maintained normal cholesterol/triglycerides.
- Humans: 52 fat patients; 10 of them had antibodies to SMAM-1, and weighed 33 pounds more than uninfected patients. They had normal cholesterol/triglycerides.
- Adenoviruses commonly infect people: colds, eye and stomach infections.
- Antibodies to another adenovirus (Ad-36) found in 11 percent of lean people, but in 30 percent of obese. The latter had normal cholesterol/triglycerides.
- Genes? No, an infected twin was more obese.
- Certain viruses known to impair brain’s appetite-control mechanism in hypothalamus, as seen in meningitis.
- Inflammation in obese: infectious agent has set off some sort of derangement in the body’s fat regulation.
What can we doctors do about these issues? First, help patients avoid polluted environments, which is what the UMA is trying to do with our committee’s activism. Second, encourage our patients to avoid processed foods, exercise vigorously to sweat off toxins and, if possible, take sauna baths (www.nydetox.org). Also one should avoid the unnecessary use of antibiotics, since they not only disrupt our intestinal flora but, in some cases (i.e. fluoroquinolones), increase insulin resistance (J. Family Practice 2007;56:101). It would also be helpful to discourage the use of antibiotics in farm animals, which has been curtailed in Europe, since they affect their gut flora, and thus their metabolism (British J. Nutrition 2006;96:820).
