Environmental causation of disease

Chronic diseases have been around for at least thousands of years, suggesting that a number of the proposed environmental causes for disease, like smoking, man-made toxins and junk food, are not the exclusive causes. Manifestations of both arteriosclerosis1) 2) and cardiac disease3) can be observed in mummies of ancient Egypt. Ötzi the Neolithic Iceman who lived around 3300 BC was found to have arthritis.4) According to a 2011 retrospective cohort study, people with exceptional longevity are not distinct in terms of lifestyle factors from the general population.5)

Modern suppression of immune system

Besides 20th century medical interventions in chronic disease, which overwhelmingly consist of immune suppressive drugs which reduce symptoms in individuals, there in this century the increasing and often unrecognized (or denied) assault of EMF on mass populations. 6)

Attempts to measure and deal with these problems are addressed in a whole new group of articles placed within Special Issues.

please browse following list ….

Poor diet and a lack of exercise

It has been widely hypothesized that a poor diet and a lack of exercise, are driving what the World Health Organization has termed “an obesity epidemic.”

A 2010 Reuters article stated:

After all, the leading causes of death in the developed world – cancer, heart disease, stroke, diabetes – all can be prevented to a large degree with exercise, by avoiding tobacco and by eating less fat and sugar and more fruits and vegetables.

But, a 2010 observational study found that increasing fruit and vegetable intake had a marginal impact on risk of cancer.7) According to the research if Europeans increased their consumption of fruit and vegetables by 150g a day (about two servings, or 40% of the WHO's recommended daily allowance), it would result in a decrease of just 2.6% in the rate of cancers in men and 2.3% in women. Even those who eat virtually no fruit and vegetables, the paper suggests, are only 9% more likely to develop cancer than those who stick to the WHO recommendations.

Further, even some of the most ambitious obesity intervention programs, which have gone to great lengths to increase rates of exercise and improve eating habits of a population, have been failures.

One 1999 $200,000 NIH-funded intervention, known as the Pathways program, was performed on two groups of children. Pathways involved a substantial increase in physical education programs, classes about nutrition, significant reduction in fat and calorie content of all school meals, and several other health related measures - and all as part of a randomized controlled trial, the gold standard in studies. The primary goal of the study was to reduce the rate of body fat in the intervention group, but after the three-year intervention the percent of body fat in both groups was essentially identical.8)

Studies such as these suggest that the official dietary advice given over the last decades do nothing to curb the increase in obesity. But just as the lack of effect of using a 10 day course of penicillin for the treatment of an L-form bacteriaDifficult-to-culture bacteria that lack a cell wall and are not detectable by traditional culturing processes. Sometimes referred to as cell wall deficient bacteria. infection is not evidence of antibiotics not being helpful in the treatment of L-form bacteria, neither is one specific life style intervention evidence of lifestyle measures not having effect.

Other interventions, such as a change in the amount and type of carbohydrate, have shown much greater promise.9) 10) 11) 12) 13) 14) 15)

Attrition was high in most of these studies, as they usually are in any kind of long term diet studies where major diet components are changed. Therefore these studies are just as much a test of the patients’ motivation and the skills of the health professional giving them advice as a pure diet test.

The mechanisms behind the effects of a low carbohydrate, - or a low glycemic, diet on weight loss are generally believed by the authors of the studies foremost to be a result of a reduced insulin secretion. Indeed, insulin administration leads to weight gain16) and insulin suppression leads to weight loss.17)

There could however be other mechanisms at play for the effects of a low-carbohydrate diet, such as changes in the body’s (gut) microbiotaThe bacterial community which causes chronic diseases - one which almost certainly includes multiple species and bacterial forms.. 18)(Note the sharper increase in Bacteriodetes on the low-carbohydrate diet in Figure 1.)

In another study, the relative level of the bacterium Selenomonas noxia in the oral cavity was able to predict obesity with a larger than 98 per cent certainty.19) As infection is the main cause of inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. in the oral cavity, it is interesting to note that a diet devoid of refined carbohydrates significantly reduces markers of gingival inflammation.20)

Smoking tobacco

Main article: Smoking tobacco

Smoking has been called “the single most preventable risk of disease” but the underlying disease process by which smoking is said to cause death and disease is not well-defined. However, there are several areas of study which point to the role of pathogens and modulation of the immune response in the diseases caused by smoking:

  • Pathogens have been detected in cigarettes.21)
  • Smoking has been shown to contribute to delayed apoptosis of immune cells as well as decrease production of antimicrobial peptides. Some evidence has emerged that smoking offers sick people symptomatic relief – through immunosuppression,22) an anti-inflammatory effect,23) or any number of other possible mechanisms.
  • Sick people are less likely to quit smoking, which may artificially inflate estimate of the harmful effect of tobacco. For example, schizophrenic patients, have reported that they smoked “primarily for sedative effects and control of negative symptoms of schizophrenia.”24) Symptomatic relief may also explain why people with mental illness are twice as likely to smoke than people without a mental illness.25)

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Toxic chemicals

Related article: Detoxification

In contrast to infectious agents, little evidence implicates typical doses of dietary chemicals as primary causes of human cancer, probably because humans have evolved effective flexible enzymatic systems for degrading potentially carcinogenic chemicals.26) Even aflatoxins, which are one of the most carcinogenic of dietary constituents, may exert their negative effects largely in conjunction with viral infection27) such as the hepatitis C virus.28)

Notes and comments

Sallie Q 03.13.2017 to follow up Smoke from wood burning heaters may be included in toxic chem?

need new section on Other environmental suppressants to contain Electrosmog and autoimmune disease Trevor G. Marshall and Trudy J. Rumann Heil pubmed ID 27412293

  • Legacy content

When described, may want to include in cancer and gut(?) articles

Gut. 2010 Jan;59(1):88-97. Gut microbes define liver cancer risk in mice exposed to chemical and viral transgenic hepatocarcinogens.29)

Fox JG, Feng Y, Theve EJ, Raczynski AR, Fiala JL, Doernte AL, Williams M, McFaline JL, Essigmann JM, Schauer DB, Tannenbaum SR, Dedon PC, Weinman SA, Lemon SM, Fry RC, Rogers AB. Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. Abstract BACKGROUND AND AIMS: Hepatocellular carcinoma (HCC) frequently results from synergism between chemical and infectious liver carcinogens. Worldwide, the highest incidence of HCC is in regions endemic for the foodborne contaminant aflatoxin B1 (AFB1) and hepatitis B virus (HBV) infection. Recently, gut microbes have been implicated in multisystemic diseases including obesity and diabetes. Here, the hypothesis that specific intestinal bacteria promote liver cancer was tested in chemical and viral transgenic mouse models. METHODS: Helicobacter-free C3H/HeN mice were inoculated with AFB1 and/or Helicobacter hepaticus. The incidence, multiplicity and surface area of liver tumours were quantitated at 40 weeks. Molecular pathways involved in tumourigenesis were analysed by microarray, quantitative real-time PCR, liquid chromatography/mass spectrometry, ELISA, western blot and immunohistochemistry. In a separate experiment, C57BL/6 FL-N/35 mice harbouring a full-length hepatitis C virus (HCV) transgene were crossed with C3H/HeN mice and cancer rates compared between offspring with and without H hepaticus. RESULTS: Intestinal colonisation by H hepaticus was sufficient to promote aflatoxin- and HCV transgene-induced HCC. Neither bacterial translocation to the liver nor induction of hepatitis was necessary. From its preferred niche in the intestinal mucus layer, H hepaticus activated nuclear factor-kappaB (NF-kappaBA protein that stimulates the release of inflammatory cytokines in response to infection)-regulated networks associated with innate and T helper 1 (Th1)-type adaptive immunity both in the lower bowel and liver. Biomarkers indicative of tumour progression included hepatocyte turnover, Wnt/beta-catenin activation and oxidative injury with decreased phagocytic clearance of damaged cells.

CONCLUSIONS: Enteric microbiota define HCC risk in mice exposed to carcinogenic chemicals or hepatitis virus transgenes. These results have implications for human liver cancer risk assessment and prevention. PMID: 19850960


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