Predicting the Cause of Disappearing Insects
Majid Ali, M.D.
Oxyphile-Oxyphobe Conflicts, Part Two
German Insect Biomass Diminished by 80%
If you are a European insect-eating bird, your food supply is diminished by 80%, so informed the journal Science.1 In northwest Germany , the insect biomass collected by monitoring traps in the Orbroicher Bruch nature reserve dropped by 78% in 24 years. Between 1970 and 2002, the biomass caught in the traps in southern Scotland declined by more than two-thirds. In other reports from North America, there has been a steep decline in the population of insect-feeding birds, including larks, swallows, and swifts. It seems safe to predict that the phenomenon of “shrinking insect biomass” will become a deepening global threat with passing year.
The mass insect disappearance has been attributed, without consensus among researchers, to shrinking insect habitat, pesticides (especially of the neotinimide type), climate change, electromagnetic fields, and light and noise pollution. This was entirely expected because the same factors had been erroneously blamed for disappearing frogs, butterflies, bees, and bats. Then the author predicted that those mass mortalities would be proven to be due to victory of oxyphobic (oxygen-shunning) fungi over oxyphilic (oxygen-loving) frogs, butterflies, bees, and bats. This indeed proved to be the case with continued research in the field.
Now the author predicts that the shrinking insect biomass worldwide will also eventually be determined to have resulted from insects becoming victims in oxyphilic-oxyphobic conflicts between oxyphobic fungi and oxyphilic insects. I explained the scientific basis and rationale of my prediction in recent comments e-published by the journal Nature reproduced below:
Fungal Pathogens and oxyphile – oxyphobe conflicts
Stegen et. al. show a collapse without recovery of a Belgian population of fire salamander (Salamandra salamandra) with arrival of fungus Batrachochytrium salamandrivorans. (ref. 1) In the combined characteristics of the fungal disease ecology, they see the potential of a ‘perfect storm’ in which it is likely to rapidly extirpate susceptible salamander populations across Europe. Without an available option, they recognize ex-situ conservation as the only viable alternative. For the United States and other regions currently considered to be free of the fungus, prevention of introduction must be based on a clear understanding of the host-pathogen dynamics as well as availability of resistant or less susceptible reservoir host species for the pathogen.
This writer recognizes the relevance and importance of the Stegen paper to the work of physicians. Fungal epidemics usually do not hold public interest for long. This has been so as well with medical practitioners who are clinically involved with fungal pathogens. This seems odd since physicians, by and large, do recognize important clinical differences between fungal and non-fungal infections. Historically, much was learned from non-fungal epidemics and some inferences could have been drawn concerning human disease from the past fungal epidemics involving bees, bats, and butterflies. Specifically, the examples of well-publicized large scale destructions of species include mass destruction of bats (with the white-nose syndrome caused by the fungus Pseudogymnoascus destructans, ref. 2), honey bees (collapsing colony disease caused by Nosema ceranae, ref. 3), and large scale disappearance of Monarch butterflies (by mycorrhizal fungi, ref. 4). Now Stegen and colleagues reveal a much deeper dimension of fungal pathogens. They also point out that the same fate of American salamander species may be expected when the fungus is introduced to the country. For these and other reasons, in this writer?s view the Stegen paper raises important questions not only about damage inflicted by fungal pathogens in the wild but also for humans.
Chytridiomycota are aquatic fungi that also thrive in the capillary network around soil particles. They are notable for their: (1) pathogenicity for amphibians; and (2) inhibition by amphibian cutaneous flora. However, this defense, as shown by Stegen et. al., does not protect fire salamander from Batrachochytrium salamandrivorans. The matter of such protection by the cutaneous flora of some amphibian species should be of interest to clinicians in considerations of host resistance.
In Altered States of Bowel Ecology (1980), (ref. 5), this writer addressed the matter of systemic symptom-complexes which clinically respond to measures that reduce the total load of fungal species in the gut flora. That led to his interest in gut immunopathology and studies of IgE antibodies in tissues and IgG antibodies in the blood with specificity for fungal antigen. (ref.6,7) This work and his parallel interest in the molecular biology of oxygen, (ref.8-9) led him to questions concerning host-pathogen dynamics among oxygen-consuming human cells (‘oxyphiles’) and oxygen-shunning fungal organisms in human ecosystems (‘oxyphobes’).(ref.10,11) These ?oxyphile-oxyphobe conflicts? ? it seemed to him ? represent a different dimension of clinical mycology that is ecologically oriented, bioenergetically directed, and therapeutically mindful of the influence of prevailing oxygen and oxygen-related conditions in the body ecosystems, especially those of the gut, blood, and liver. (ref. 9-11)
The recent report of incremental loss of oxygen from oceans (ref.12) is noteworthy in this context and so are the incremental oxidizing capacity of the planet Earth and the cumulative chemical load on its the ecosyetems. (ref.13) Might these factors be of importance in considerations of immunosuppression in our species? If so, might the matters of oxyphil-oxyphobe conflicts be clinically significant in the prevention and treatment of fungal overload and infections? Should physicians not think ecologically? Should they not be mindful of the state of oxygen homeostasis in their patients for health preservation and disease prevention?
The work of Stegen et al. is clearly of relevance to physicians’ work.
1. Stegen G, Pasman F, Schmidt BR, et al. Drivers of salamander extirpation mediated by Batrachochytrium salamandrivorans. Nature. 2017;544:353.
2. Stone, WB. Bat white-nose syndrome: An emerging fungal pathogen. Science. 2009;323:227.
3. Higes M, Martin R, Meana A. Nosema ceranae, a new microsporidian parasi te in honeybees in Europe. J Invert Pathol. 2006;92:93?95.
4. Lef�vre T, Oliver L, Hunter MD, et al. Evidence for trans- generatilonal medication in nature. 2010;13:1485-1493.
5. Ali M. Altered States of Bowel Ecology. (monograph). Teaneck, NJ, 1980.
6. Ali Ali M, Mesa -Tejada R, Fayemi AO, Nalebuff DJ, Connell JT: Localization of IgE in tissues by an immunoperoxidase technique. Arch Pathol Lab Med, 103:274-275, 1979.
7. Ali M. Ramanarayanan MP, Nalebuff DJ, Fadal RG, Willoughby JW: Serum concentrations of allergen-specific IgG antibodies in inhalant allergy: effect of specific immunotherapy. Am J Clin Pathol, 80:290-299, 1983.
8. Ali M. Respiratory-to-Fermentative (RTF) Shift in ATP Production in Chronic Energy Deficit States. Townsend Letter for Doctors and Patients. 2004;253:64-65.?
9. Ali M. Succinate Retention: The Core Krebs Dysfunction in Immune-Inflammatory Disorders. Townsend Letter. 2015;388:84-85. Succinate retention.
10. Ali M. Darwin, Dysox, and Disease. Volume XI. 3rd. Edi. The Principles and Practice of Integrative Medicine.2008. New York. (2009) Institute of Integrative Medicine Press.
11. Ali M. Darwin, Dysox, and Integrative Protocols. Volume XII. The Principles and Practice of Integrative Medicine. New York (2009). Institute of Integrative Medicine Press.
12. Schmidtko S, Stramma L, Visbeck M. Decline in global oceanic oxygen content. Nature 20117;543:335-339.
13. Gupta ML, Perturbation to global tropospheric oxidizing capacity due to latitudinal redistribution of surface sources of NOx, CH4 and CO. Geographical Research Letters. 1998;25:3931-3934.