Silver – Entering the real battle against resistant bacteria?

Due to the continuing progression of antibiotic resistant bacteria development in the medical community a number of individuals believe it is time to explore how to incorporate silver, a long standing antibacterial agent, into treatment strategies. On its face this appears to be an important new avenue for attacking the growing problem of resistant bacteria and the lack of development of new antibiotics to fight these bacteria. However, this excitement must be stemmed by appropriate knowledge of how silver helps fight bacterial infections and the potential pitfalls to its incorporation into actual antibiotics or other blood based treatment strategies versus its current medical uses as a sterilization and wound dressing tool.

The use of silver in medical and wound management dates back to the 18th century with the application of silver nitrate to treat ulcers.1,2 Anti-microbial activity for silver ions was first scientifically suspected in the 19th century, although anecdotal reasoning can be traced back much earlier.3 However, in the early 20th century the overall effectiveness of penicillin and later discovery of other antibiotics displaced silver use for over two decades. Silver use increased in the 1960s in response to burn treatments through the use of a silver sulfadizine (SSD) cream. In modern times silver is incorporated into wound dressings, antibiotic cream and first-aid plasters to reduce bacterial growth and limit infection.4,5

Both bulk silver and isolated silver nano-particles are effective at killing, not only standard Gram-negative and Gram-positive bacteria, but also antibiotic-resistant strains.6-8 This action also catalyzes antibacterial activity of current antibiotics including penicillin G, amoxicillin, erythromycin, clindamycin, and vancomycin.9 Various mechanisms have been suggested to explain the anti-microbial action of silver: 1) particle penetration of bacterial cell walls and membranes leading to DNA damage and apoptosis possibly due to free radical incursion; 2) alteration of bacterial cell wall and membrane, most likely targeting lipopolysaccharides, forming pits increasing membrane permeability for antibiotics or disrupting respiration for aerobes; 3) lowering probability of biofilm formation increasing the probability of antibiotic effectiveness.10-13

There is no clear evidence regarding whether the anti-microbial effects of silver are found in colloidal silver or ionic silver or both, but some evidence suggests that colloidal silver is much less effective as an anti-microbial agent than ionic silver, especially because only oxidized silver nanoparticles exert a significant antibacterial effect.14,15 If colloidal silver has anti-microbial action its magnitude is largely dictated by the dimensions of the particles where smaller particles have a greater effect due to higher surface area to volume ratios.16-18 The shape of the nano-particle also seems important with truncated triangles having superior activity.19,20

Ionic silver is thought to activate its anti-microbial effects through the formation of complexes with negatively charged sulfur, nitrogen or oxygen functional groups in bacterial enzymes destabilizing the bacteria and preventing normal functions like metabolism and reproduction.15,21 So silver nano-particles may simply be an inert element that eventually degrades creating the actual silver anti-microbial agent with degradation occurring faster at smaller sizes and certain shapes. Therefore, when studying anti-microbial activity and possible silver toxicity it stands to reason that one should focus on oxidized silver versus neutral silver.

While the anti-bacterial properties of silver were suggested in the 19th century, silver resistant bacteria and the basis for that bacterial resistance was first reported much later in 1975, first in Salmonella typhimurium.22,23 This resistance is chiefly born from plasmid development or transfer.24,25 The chief silver resistant plasmid has been labeled pMG101, is 180-182 kb with nine Open Reading frames (seven known and two unknown) in three transcriptional units and like most plasmids is conjugally transferable between bacteria.24,26 In addition to silver, pMG101 grants additional resistance to mercury, tellurite, ampicillin, chloramphenicol, tetracycline, streptomycin, and sulphonamide as well.23,24,27 Note the wide variety and importance of this resistance against not only silver, but other frequently used antibiotics. pMG101 presence can resist up to six times minimum silver lethality for E. coli and more than likely other bacteria species.24,27

Overall silver resistance is driven by encoding two silver efflux pumps (one an ATPase and the other chemiosmotic) and two periplasmic Ag+-binding proteins.26 Basically silver ion uptake is decreased and silver efflux is increased. There is also some belief that an ATP-dependent copper efflux protein can mediate removal of silver ions.1 However, there is no direct evidence that this silver resistance mechanism induces cross-resistance to various antibiotics, but the rate of cross-resistances to other antibiotics and genetic linkage of silver resistance and antibiotic resistance genes provides positive circumstantial evidence.

Various bacteria species that have been identified as having silver resistance are E. cloacae, Enterobacteriaceae, Salmonella typhimurium, Klebsiella pneumoniae, Pseudomonas stutzeri, P. aeruginosa and E. coli.27-35 Resistance is principally generated through sil genes (one of the genes contained in the pMG101 plasmid) with its functions having been assigned due to homologous genes that encode resistance to other genes.22 However, there is question regarding the total level of silver resistance provided by sil genes because some research has demonstrated only partial phenotypic silver resistance, thus providing only partial resistance to silver.22,28,29 The reason for this partial resistance could be driven by lack of complete transcription due to a lack of consistent silver forcing selection pressure. Finally silver resistance has developed from acinetobacter baumannii based on seemingly separate 54 kb plasmid (pUPI199).31

Despite the variety of bacteria that can acquire silver resistance, the high-level and multi-faceted mode of action from silver (cell wall destruction and reduced antibiotic efflux) lead most to believe that the development of silver resistant is unlikely. While silver resistant bacteria appear rare, one of the reasons for this rarity is thought to be that silver is not utilized at high levels for antibacterial purposes similar to current antibiotics and if this were to change so would the rates of silver resistance development.

One of the big problems with regards to determining an accurate accounting of silver resistance is the lack of standardized metrics for this resistance. There is disagreement on the MIC50 breakpoints for bacteria susceptibility.34 When most silver microbial susceptibility studies are performed the conducting researchers tend to assign their own breakpoints to delineate susceptible and resistant strains. For example results from studies that explored MIC values for Staphylococcus aureus ranged from 8 to 80 mg/L32,33 where studies for Pseudomonas aeruginosa produced a range between 8 and 70 mg/L.34,35

Another problem is a general lack of standardization for silver ion anti-microbial testing methods mostly driven by solubility issues that change the rate of available silver ions due to formation of various silver-halide anionic complexes.1 This influence is most noted in the sodium chloride content of the microbiological medium used for susceptibility testing.1 Also the lack of standardization in silver wound dressings creates numerous delivery systems to release silver ions, which include elements beyond simple silver concentration to influence the ability to kill microorganisms.36 These discrepancies create questions regarding how different tests can be compared for similarities or differences in method.

One of the principle concerns with incorporating silver into antibiotic treatments that directly enter the blood is the potential for serious negative side effects. There are three important factors that govern the ability of a metal to produce systemic toxic effect: 1) the rate of absorption due to the solubility of the metal; 2) the capacity to bind to biological targets in the body; 3) the residence time of the metal after absorption both at biological targets and in the blood stream before elimination through excretion. The form of silver that is introduced to the body influences these three elements. Currently silver is largely applied as either silver nitrate (inorganic silver salts) or as organic compounds like SSD.1

Normal (no medical or heavy industry work) silver concentration in the body is very low with <2.3 ug/L (or 3 nmol/L) in the blood, about 2 ug/day (or < 8 nmol/L) expelled in urine and 0.05 ug/g (wet tissue) in the liver and kidneys.37-39 Some evidence has demonstrated that some SSD treated burn patients have plasma silver concentrations as high as 50 ug/L after 6 hours of treatment and can reach a maximum of 310 ug/L.37 In one particular case a patient that died of renal failure after 8 days of treatment had silver concentrations of 970 ug/g, 14 ug/g and 0.2 ug/g in the cornea, liver and kidney respectively.37,38 Due to silver derived renal toxicity from topical application (from wound bandages) most physicians believe that it is improper to apply topical silver treatments over long periods of time even on burn patients.

However, despite the above information most believe that silver application is generally safe with accumulation occurring in superficial layers of the liver and kidneys with full clearance after 28 days.39,40 Such limited consistent binding and the rate of clearance implies superficial binding and low absorption from a single application. However, there is limited information regarding how organ absorption would change with direct silver application to the blood.

Overall there are still numerous safety and toxicity studies that must be performed before even considering applying silver directly to oral or intravenous antibiotic treatments. Also new policy limiting the application of ionic silver, in either direct or indirect form, to non-medical products for an anti-microbial agent must be created because mass application dramatically increases the probability for widespread resistance development. Such an outcome has already occurred for numerous existing antibiotics and based on the apparent resistance profile for sil genes and their corresponding plasmids the widespread development of silver resistant bacteria could create a pathogen that cannot be effectively managed through modern medicine.

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Citations –

1. Chopra, I. “The increasing use of silver-based products as antimicrobial agents –a useful development or a cause for concern?” Journal of Antimicrobial Chemotherapy. 2007. 59:587-590.

2. Klasen, H. “Historical review of the use of silver in the treatment of burns. I. Early uses.” Burns. 2000. 26:117-130.

3. Hugo, W, and Russell, A. “Types of antimicrobial agents. In: Russell, A, Hugo, W, Ayliffe, GAJ eds. Principles and Practice of Disinfection, Preservation and Sterilisation. Oxford, UK: Blackwell Scientific Publications: 1982. 8-106.

4. Fox, C Jr, “Silver sulfadiazine – a new topical therapy for Pseudomonas in burns. Therapy of Pseudomonas infection in burns.” Arch Surg. 1968. 96:184-188.

5. George, N, Faoagali, J, and Muler, M. “Silvazine (silver sulfadiazine and chlorhexidine) activity against 200 clinical isolates.” Burns. 1997. 23:493-495.

6. Burrell, R, et Al. “Efficacy of silver-coated dressings as bacterial barriers in a rodent burn
sepsis model.” Wounds. 1999. 11:64-71.

7. Yin, H, Langford, R, and Burrell, R. “Comparative evaluation of the antimicrobial activity of ACTICOAT anti-microbial barrier dressing.” J Burn Care Rehabil. 1999. 20:195-200.

8. Percival, S, Bowler, P, and Dolman, J. “Anti-microbial activity of silver-containing dressings on wound microorganisms using an in vitro biofilm model.” Int Wound J. 2007. 4:186-191.

9. Shahverdi, A, et Al. “Synthesis and effect of silver nanoparticles on the antibacterial activity of different antibiotics against Staphylococcus aureus and Escherichia coli.” Nanomedicine. 2007. 3:168-171.

10. Sondi, I, and Salopek-Sondi, B. “Silver nanoparticles as anti-microbial agent: A case study on E. coli as a model for Gram negative bacteria.” J Colloid Interface Sci. 2004. 275:177-182.

11. Hwang, E, et Al. “Analysis of the toxic mode of action of silver nanoparticles using stress-specific bioluminescent bacteria.” Small. 2008. 4:746-750.

12. Kim, J, et Al. “Anti-microbial effects of silver nanoparticles.” Nanomedicine. 2007. 3:95-101.

13. Morones-Ramirez, J, et Al. “Silver Enhances Antibiotic Activity Against Gram-Negative Bacteria.” Sci. Transl. Med. 2013. 5:190ra81.

14. Alvarez, J, et Al. “Negligible particle-specific antibacterial activity of silver nanoparticles.” Nano Lett. 2012. 12:4271−4275.

15. Lok, C, et Al. “Silver nanoparticles: Partial oxidation and antibacterial activities.” J Biol Inorg Chem. 2007. 12:527-534.

16. Baker, C, et Al. “Synthesis and antibacterial properties of silver nanoparticles.”
J Nanosci Nanotechnol. 2005. 5:244-249.

17. Panacek, A, et Al. “Silver colloid nanoparticles: Synthesis, characterization, and their antibacterial activity.” J Phys Chem B. 2006. 110:16248-16253.

18. Guzman, M, Dille, J, and Godet, S. “Synthesis of silver nanoparticles by chemical reduction method and their antimicrobrial activity.” Proceedings of World Academy of Science, Engineering and Technology. 2008. 33:367–74.

19. Pal, S, Tak, Y, and Song, J. “Does the antibacterial activity of silver nanoparticles depend on the shape of the nanoparticle? A study of the Gram-negative bacterium Escherichia coli.” Appl Environ Microbiol. 2007. 73:1712-1720.

20. Wiley, B, et Al. “Shape-controlled synthesis of metal nanostructures: The case of silver.” Chem Eur J. 2005. 11:454-463.

21. Damm, C, Munstedt, H, and Rosch, A. “Long-term antimicrobial polyamide silvernanocomposites.” J Mater Sci. 2007. 42:6067–73.

22. Woods, E, Cochrane, C, and Percival, S. “Prevalence of silver resistance genes in bacteria isolated from human and horse wounds.” Veterinary Microbiology. 2009. 138(3-4):325-344.

23. McHugh, G, et Al. “Salmonella typhimurium resistant to silver nitrate, chloramphenicol, and ampicillin.” Lancet. 1975. 1(7901):235-40.

24. Gupta, A, Maynes, M, and Silver S. “Effects of halides on plasmid-mediated silver resistance in Escherichia coli.” App. Environ. Microbiol. 1998. 64(12):5042-5.

25. Davis, I, Richards, H, and Mullany, P. “Isolation of silver- and antibiotic-resistant Enterobacter cloacae from teeth.” Oral Micro and Immunol. 2005. 20(3):191-4.

26. Silver, S. “Bacterial silver resistance: molecular biology and uses and misuses of silver
363 compounds.” FEMS microbiol rev 2003. 27(2-3):341-53.

27. Gupta, A, et Al. “Molecular basis for resistance to silver cations in Salmonella.” Nature Med. 1999. 5(2):183-188.

28. Annear, D, Mee, B, and Bailey, M. “Instability and linkage of silver resistance, lactose fermentation, and colony structure in Enterobacter cloacae from burn wounds.” J. Clin Pathol. 1976. 29:441-443.

29. Hendry, A, and Stweart, I. “Silver-resistant Enterobacteriaceas from hospital patents.” Canadian J. Microbiol. 1979. 25:915-921.

30. Bridges, K, et Al. “Gentamicin and silver-resistant Pseudomonas in a burns unit. Br. Med. J. 1979. 1:446-449.

31. Deshpande, L, and Chopade, B. “Plasmid mediated silver resistance in Acinetobacter baurmannii.” Biometals. 1994. 7:49-56.

32. Ug, A, and Ceylan, O. “Occurrence of resistance to antibiotics, metals and plasmids in clinical strains of Staphylococcus spp.” Arch. Med Res. 2003. 34:130-136.

33. Hamilton-Miller, J, Shah, S, Smith, C. “Silver sulphadiazine: a comprehensive in vitro reassessment.” Chemotherapy. 1993. 39:405-409.

34. Vassishta, R, Chhibber, S, Sexena, M. “Heavy metal resistance in clinical isolates of Pseudomonas aeruginosa.” Folia Microbiol (Praha). 1989. 34:448-452.

35. De Vicente, A, et Al. “Resistance to antibiotics and heavy metals of Pseudomonas aeruginosa islated from natural waters.” J. Appl Bacteriol. 1990. 68:625-632.

36. Thomas, S, and McCubbin, P. “A comparison of the anti-microbial effects of four silver-containing dressings on three organisms.” J. Wound Care. 2003. 12:101-107.

37. Wan, A, et Al. “Determination of silver in blood, urine, and tissues of volunteers and burn patients.” Clin Chem. 1991. 37(10 Pt 1):1683–1687.

38. Boosalis, M, et Al. “Serum and urinary silver levels in thermal injury patients.” Surgery. 1992. 101(1):40–43.

39. Coombs, C, et Al. “Do burn patients have a silver lining?” Burns. 1992. 18(3):179–184.

40. Harrison, H. “Pharmacology of sulfadiazine silver. Its attachment to burned humans and rat skin and studies of gastrointestinal absorption and extension.” Arch Surg. 1979. 114(3):281-285.

Looking for the Truth Behind the Health Value of Saturated Fat versus Carbohydrates

One of the more dynamic areas of modern research is nutrition and how it relates to biology. While in the past the more popular medium of discussion was through various diet/weight loss books, now the question of saturated fats and their overall influence on health has shifted to areas of more stringent study. Through most of the modern age of nutrition it has been viewed by the majority that saturated fats were largely negative and should be avoided as much as possible. Even the USDA recommends less than 10% of calories be derived from saturated fats1,2 largely based on the premise that increasing saturated fat consumption increases detrimental health outcomes including cardiovascular heart disease (CHD).3-5 However, there are individuals that believe this recommendation is inappropriate for it has not been clearly demonstrated empirically that increased consumption of saturated fat increases CHD or other negative health outcomes.

In fact some cite that while increasing saturated fat does increase total cholesterol, which is a characteristic for an increased rate of CHD, the rate of increase for high density lipoprotein (HDL) exceeds the rate of increase for low density lipoprotein (LDL), thus increasing the HDL/LDL ratio which is thought to be a more important factor to overall health than total cholesterol.6 Therefore, in the eyes of these individuals increasing saturated fatty acid (SFA) consumption in an equal caloric substitution over other types of nutrients like carbohydrates does not increase CHD risk and may even lower it.7-10 Overall the problem with both positions regarding the health effects of saturated fat is that most analysis fails to appreciate the specificity that addressing such an issue demands.

The crux of the question does involve the level at which one consumes saturated fats, but there are four central questions that govern the importance of that change:

First, different individual SFAs do not have the same biological effects despite similar molecular constructs. For example some epidemiological evidence demonstrates that stearic acid is the most detrimental SFA in terms of increasing the probability of CHD.11 Also despite the difficulty distinguishing between the overall effects of different SFAs palmitic acid is thought to be more detrimental to overall health than lauric acid. Not surprisingly in overall cholesterol raising effects stearic acid is neutral while all other long-chain acids increase both HDL and LDL levels versus low quality carbohydrates.12 There are no definitive conclusions regarding the influence of short and medium-chain SFAs due to a lack of study.

One of the reasons stearic and palmitic acid are so bad is that they can provide a negative feedback on acetyl-CoA carboxylase (ACC), the enzyme responsible for the catalysis of acetyl-CoA to malonyl-CoA which is utilized to increase the size of acyl chains reducing palmitic acid processing.13 In some respects there is little difference between trans-fatty acids and these two SFAs.

One would anticipate that it would be difficult to separate different types of SFAs with respect to what foods an individual consumes due to the combination of various SFAs in foods. However, it is feasible to distinguish certain specific foods that have higher percentages of certain SFAs over others and make broad dietary suggestions about those food items. For example palm oil and coconut oil have very high in palmitic and lauric acid concentrations respectively. Therefore, when studying the difference between SFAs and carbohydrates it is important to track what foods are consumed to ensure objectivity regarding certain SFA specific overload foods.

Second, when changing the amount of consumed SFAs some other molecule will replace those calories, thus it is important to consider the nature of that replacement and its specificity. Of the four issues that will be discussed this issue of substitution is the most studied one. There are a wide variety of elements that can replace saturated fat in a diet: protein, poly-unsaturated fat, mono-unsaturated fat, high glycemic index (low-quality/processed) carbohydrates, low glycemic index (high-quality) carbohydrates, “normal”/unsaturated fat and trans fats. Preliminary studies support the belief that rates of CHD decrease when replacing SFAs with poly-unsaturated fat, mono-unsaturated fat and “normal” fat.3,14,15 CHD rates increase when replacing SFAs with trans fats and refined/processed carbohydrates.3,16 Note that the glycemic index is utilized to measure how quickly blood sugar rise after consuming a given food and uses glucose as a upper level (100).

However, with regards to the carbohydrates since a large number of the carbohydrates that are consumed in modern society are of high glycemic variety if one were to guess it stands to reason that most, if not all, carbohydrate studies involved processed carbohydrates instead of quality carbohydrates. For example some proponents of SFAs like to cite studies that conclude a switch from SFAS to carbohydrates increases CHD probability. However, these studies do not typically differentiate between carbohydrate types. There is a large biological difference between low glycemic and high glycemic carbohydrates; without differentiating between carbohydrates any results born from substituting SFAs with a caloric equivalent amount of carbohydrates are inherently suspect. Think of it this way anyone who concludes that there is no biological and nutritional difference between consuming 150 calories of traditional rolled oats oatmeal versus 150 calories of Twinkie should not have their opinion taken into consideration.

In addition substitution studies must take appropriate caloric equivalency into account. For example if SFAs makes up 300 calories of a person’s daily caloric intake suitable comparison would demand that some percentage of that value be replaced with an equal value of the replacement (carbohydrates, poly unsaturated fat, etc.). It is sometimes difficult to track this equivalency feature if individuals are simply trying to recall what they consume over a given period of time versus keeping a food diary and having nutritionists correct for imbalances. Finally there is almost no information pertaining to replacing SFAs with protein or low glycemic index carbohydrates with regards to influence on CHD rates further limiting the value of substitution studies, an important exclusion that must be corrected for a definitive statement can be made regarding substitution. In the current environment the burden of proof is on those that believe SFAs are neutral or even better for health than processed carbohydrates, thus they need to ensure the quality of these substitution studies if they want to make the above contention.

Third, one of the biggest problems with comparing health effects between consumption of different food elements is a lack of comparison between subject microbiota. In short the microbiota is the concentration and type of bacteria population in an individual’s gastro-intestinal system. Numerous studies have demonstrated that the type of bacteria in an individual’s intestinal system have a significant impact on the ability to process and absorb nutrients.17-21 One of the biggest comparisons in microbiota is between Firmicutes and Bacteroidetes, which generally identifies obese individuals and non-obese individuals where Firmicutes is at larger concentrations in the obese and Bacteroidetes is at larger concentrations in the non-obese, usually with a 100%+ change.17,18 Note that this relationship is obviously not perfect, but is generally a good rule of thumb.

Evidence has shown that prolonged high SFAs feeding induced inflammation, impaired barrier function and changed microbiota profiles.22 The change in profiles lead to increased concentrations of Firmicutes and Oscillibacter and reduced concentrations of Bacteroidetes and Lactobacillus, thus high SFA feedings change the microbiota to one more seen in obese individuals. Clearly obesity is known for numerous detrimental health conditions, thus possessing a similar microbiota can be rationally viewed as a detrimental outcome versus a beneficial one.

Gut microbiota is important relative to carbohydrate processing as well in the rates and what types of carbohydrates are digestible.23,24 Fermentation occurring in the gut also leads to an increase in GLP-1 synthesis and insulin metabolism, thus rats fed a high fiber diet have higher plasma GLP-1, insulin and c-peptide levels after an oral glucose load.17 Various bacteria breakdown carbohydrates in fermentation reactions producing short chain fatty acids (SCFAs) like acetate, propionate and butyrate.25 Butyrate largely provides energy for colonic epithelia, propionate is taken up by the liver and is a precursor for gluconeogenesis, protein synthesis and liponeogenesis26,27 and acetate is metabolized by peripheral tissues and used as a substrate for cholesterol synthesis.28

The ratio of which SCFAs are produced is largely dependent on the ratio of bacteria in the gut. Evidence suggests that Firmicutes is able to produce about 25% more SCFAs than Bacteroidetes.19,20 Firmicutes appears to produce more butyrate and propionate with Bacteroidetes producing more acetate.29 There is question whether or not higher amounts of SCFAs are linked to obesity, but the evidence favors the affirmative: that increased SCFAs increase obesity probability.18,21,30 Also Firmicutes may increase the rate of malonyl-CoA activation over Bacteroidetes, which reduces the rate of carnitine palmitoyl transferase-1 reducing the amount of mitochondrial fatty acid oxidation.31 Overall while there is still a lot of information that needs to be deduced from the relationship between microbiota and health in general, especially obesity, the exclusion of any relationship in substitution studies is inappropriate.

Fourth, with regards to carbohydrate substitution, physical and aerobic conditioning of the research subject must be taken into consideration. Consistent exercise results in the increased direct and indirect consumption of carbohydrates as an energy source. Indirect consumption occurs through the increased production of specific enzymes, which favor the conversion of certain carbohydrates to glycogen versus SFAs like stearic or palmitic acid. Basically if one is substituting carbohydrates for SFAs in overweight and/or inactive research subjects the biological reduction of SFA consumption is heavily handicapped because the substituted carbohydrates are less likely to be used as short-term energy, but instead are converted to SFAs for long term energy storage.

One of the important elements when distinguishing between biological effects of SFAs and carbohydrates is the synthesis and consumption of glycogen. Glycogen is a multi-branched polysaccharide consisting of various glucose derivative molecules bound together and is used for long-term energy storage in a more compact form over triglycerides.

Glycogen is principally isolated within muscles, the liver and red blood cells32,33 and its rate of storage is dependant on physical training, basal metabolic rate and eating habits. Storage begins when blood glucose levels rise and insulin concentrations increase stimulating the action of hepatocytes leading to glycogen synthesis. As long as glucose and insulin remain in high relative concentrations glycogen synthesis continues. In periods of low glucose the pancreas secretes glucagons which catalyzes glycogenolysis.

Not surprisingly glycogen synthesis is exogonic, where UTP reacting with glucose-1-phosphate to drive the formation of UDP-glucose that eventually combine to lengthen glycogen through catalyzation by glycogen synthase forming from a base created by glycogenin.33 Glycogen consumption is endergonic where sections are cleaved by glycogen phosphorylase to produce glucose-1-phosphate monomers, which are later converted to glucose-6-phosphate by phosphoglucomutase. Glucose-6-phosphate produced from glycogen can enter the glycolysis pathway, the pentose phosphate pathway or be dephosphorylated back to glucose.33

A history of exercise, especially endurance training, enhances lipid and carbohydrate oxidation and decrease SNS activity during present time exercising in part due to increased muscle glycogenolysis and increased recruitment of skeletal muscle.34-38 Increasing exercise intensity increases the level of energy demand from the muscles and brain resulting in a faster crossover from lipids to carbohydrates as a source of energy. While some believe that there are special exercise-dietary regimens to enhance muscle glycogen storage/consumption rates when appropriate, there is no doubt that individuals who exercise consistently have higher rates of glycogen conversion of glucose and other sugars versus rates of glucose conversion to SFAs opposed to the rates found in overweight or obese individuals.34,39,40

One of the advantages of this difference is in the short period of time after exercise (24 hrs) is that rate of glycogen synthesis is indiscriminate the type of carbohydrate, be it simple or complex.40 Note that there is still an insulin concentration rise for simple carbohydrates over complex, but while the increase for complex is smaller the duration is longer.40 The fate of consumed carbohydrates is also influenced by the time between consumption and exercise.41 Therefore, individuals that are “in shape” are more likely to burn off consumed carbohydrates versus storing them as either glycogen or SFAs. Again comparison studies between SFAs and substitutions, especially carbohydrates, tend to exclude the influence of exercise.

Another side issue that must be considered when making comparison studies between SFAs and substitutes is the concentration of epinephrine due to its lipolytic, glycogenolytic and insulin-suppressive effects.42 Past training through exercise seems to reduce epinephrine concentrations in both at rest and during present exercise.42,43 Therefore, measurement of epinephrine needs to be conducted to act as a control point to make more accurate comparisons in substitution studies.

Overall there are clearly scientific and accuracy concerns regarding claims made by individuals who believe that SFAs are no more harmful to CHD rates than carbohydrates. Unfortunately such claims are typically made by individuals who are trying to justify a certain nutritional lifestyle versus individuals who actually care about proper nutrition. This is not to say that all forms of carbohydrates are guaranteed to be healthier than SFAs; the problem is that SFAs proponents have not produced evidence to demonstrate this conclusion that satisfies the four above concerns. Therefore, until this evidence is produced it is irresponsible of individuals to suggest that substituting SFAs for carbohydrates produces no detrimental change to CHD rates.


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Citations –

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2. U.S. Department of Agriculture (USDA) Food Guide or the Dietary Approaches to Stop Hypertension (DASH) Eating Plan. http://www.unco.edu/shc/topics/dietaryguidelines.htm

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13. Wikipedia - Palmitic acid Entry.

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24. Goodlad, R, et Al. “Proliferative effects of 'fibre' on the intestinal epithelium: relationship to gastrin, enteroglucagon and PYY.” Gut. 1987. 28(Suppl): 221-6.

25. Macfarlane, G, and Gibson, G. “Carbohydrate fermentation, energy transduction and gas metabolism in the human large intestine.” In: Mackie RI, White BA (eds). Gastrointestinal Microbiology. Chapman & Hall: New York, USA, 1997. 269–317.

26. Wolever, T, Spadafora, P, and Eshuis, H. “Interaction between colonic acetate and propionate in humans.” Am J Clin Nutr. 1991. 53:681–687.

27. Vernay, M. “Origin and utilization of volatile fatty acids and lactate in the rabbit: influence of the faecal excretion pattern.” Br J Nutr. 1987. 57:371–381.

28. Wolever, T, et Al. “Effect of rectal infusion of short chain fatty acids in human subjects.” Am J Gastroenterol. 1989. 84:1027–1033.

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Leadership in Large Societal Movements

Numerous treatises have been written about leadership, its origins and supposedly how to develop it. Unfortunately many of these discussions are limited in importance for most people because they focus on small environments where the consequences are who gets marketing account A or wins the debate B. Even the larger environments of democratic elections are limited in their scope because of term limits and the general reversibility of a vast majority of accomplishments, be it beneficial or detrimental. The true importance of leadership comes from those attempting to lead movements against large organizations or government, especially those leaders that do not come from some form of seat of power.

The sad reality when it comes to individualized power is that it is essential to accomplishing anything substantial over a long period of time without resorting to violence. Some may take offense to this statement citing numerous events in history where the “downtrodden”, powerless and oppressed banded together and rose up against their oppressors without requiring violence like the civil rights movement (sans the Black Panthers) in the United States and the movements supporting India Independence. However, when looking at these events in earnest, past the “underdog” hype and mythos, those that eventually succeeded over the long-term required either the intervention of individuals with power or their apathy in fight against the movement.

For example based on known elements at the time and in the future, it is unlikely that the Civil Rights Act of 1964 would have been passed effectively codifying the success of the civil rights movement if Richard Nixon had won the U.S. presidency in 1960. Also when viewing John F. Kennedy’s unwillingness to aggressively address the “black equality” question and difficulty confronting the Southern Democrats, it can be argued that had Kennedy not been assassinated in 1963 it is unlikely the Civil Rights Act would have been passed either, at least until a much later date. Numerous people underestimate the commitment that then president Lyndon B. Johnson had towards resolving the level of inequality for blacks in the South, a commitment that was lacking in both Nixon and Kennedy. In fact a number of historians give Johnson credit for pushing the Kennedy administration to address civil rights. Clearly if Johnson had not been president at the time, granting him the ability to wield a large level of power, it is unlikely that the civil rights movement at the time would have been successful while remaining non-violent and the probability of winning when turning to violence was almost zero.

Similarly India acquired its independence from British rule largely because it was calculated that the detriments from keeping India as a colony exceeded the benefits regardless of the movement clamoring for independence. For numerous foreign “revolutions” in the modern era intervention by powerful outside parties, like the United States, is principally involved in tipping the scale for example recently in Libya, the “rebels” were on the brink of annihilation before the intervention of NATO. However, the common denominator in all of these revolutions is the administration of power, brought on by those who inherently had it or through violence.

When there is a lack of individuals with significant power and a movement elects not to resort to violence how can a movement expect to accomplish its goals? Normally it will not accomplish those goals, a result that can be seen over numerous event through history most recently in the currently failing 2nd Egyptian revolution now that the army is actually interested in maintaining the status quo and the short-lived, but highly publicized, Occupy Wall Street (OWS) movement in the United States. So is there a way for these movements to have success without applying power from the above sources?

The first critical element to any societal movement regardless of the amount of possessed power is the realization of sacrifice. Note that for the purposes of this discussion a “societal movement” is defined as: “a movement that aims to significantly influence the workings of a given society on a large scale”. OWS accomplished almost nothing worthwhile largely because the greatest level of defiance that most of its members were willing to undertake was cause a small amount of annoyance for those in certain positions of power in New York. Some could spin the accomplishments of the movement to include improved unity or societal clarity that expanded beyond New York, but those individuals are simply grasping at straws in their attempt to defend OWS. One could argue that the movement was about little more than the ego of the participants and pointless steam venting versus actually solving the problem of growing wealth inequality in the U.S. Would a legitimate devotion to sacrifice and the elimination from the movement anyone who was not willing to undertake the same mindset have changed the result?

From this presumption an interesting question arises. Suppose at the time of the OWS protest (fall of 2011) 5000 random individuals involved were asked whether or not he/she would be willing to be incarcerated for 15 years at a medium security prison in the general population in exchange for the passage of Fictional Bill 104 (FB 104). FB 104 would establish a real time maximum asset cap for individuals of 20 million dollars and for corporations a maximum yearly profit cap of 150 million dollars. The government would tax 100% of all income/earnings/wages/assets/etc over either cap. The IRS would be given much greater authority to pursue and charge tax cheats/thieves and all tax cheats found guilty would receive jail terms in medium security prisons with minimum sentences equating to 1 year per $100,000 that was concealed. Also U.S. foreign policy would place emphasis on pressuring notorious tax havens to open their books regarding banking by U.S. citizens, similar to the tactics recently used against Switzerland. Taxes accrued from this ceiling tax would be used to fund food banks, education, apprenticeships and small business loans to increase both the job pool and the number of qualified applicants.

So given this general outline of FB 104, which should go a long way to limiting the equality gap in the United States, how many of the 5000 polled protesters would actually sacrifice their freedom for 15 years to accomplish this goal? Sad to say probably not many of them, if any at all. What if unless at least 75% of those asked accept the terms the bill would not become law? Note that in the above example 15 years in prison signifies a tradeoff for the bill and is supposed to represent some of the real sacrifice that OWS protesters could have engaged in, various elements of economic disruption, which could have “persuaded” the federal government into actually doing something about the problem.

Another problem with the OWS movement was their “strategy”, if one could even say they had one, was not realistic relative to the general psychological makeup of society. While the overall initial goal, before it basically became a mouthpiece for every non-conservative societal complaint, was never fully clear; the argument against increasing financial inequality due to the application of superficial importance to certain occupations and the minimization of importance of others implies that OWS wanted the formation of a genuine meritocracy with appropriate handicap measurements for individualized starting positions. Note that the above statement is a rather mouthful so what exactly does it mean?

Most individuals are familiar with a meritocracy. A meritocracy is a school of thought that believes power and influence should be vested in individuals according to potential and accomplishment not class/rank, blood, connections, etc. In addition occupations and roles that foster positive societal development and stability take precedence over occupations that do not. For example in such an environment entertainers and stockbrokers would make considerably less money than physicians, teachers and engineers.

The appropriate handicap measurement element is basically a socio-economical version of the original premise behind affirmative action. The original idea behind affirmative action was to create an evaluation system, which extrapolated performance in similar opportunities between candidates even if only one participated in the specific opportunity. Basically certain individuals due to socio-economic, racial and/or ethnic background will not be afforded certain educational and/or occupational opportunities. Note that the “not” in the previous sentence is important because these individuals did not fail at the opportunity or fail to accept the opportunity, but never had the option of accepting the opportunity in the first place.

The key aspect of affirmative action was to use the written information (usually in the resume or other requested items) to create an effective questioning session for the interview to extract the necessary information to make the comparison extrapolation. Unfortunately for whatever reason, more than likely simple laziness, this original intent has devolved into quasi-quota systems (because actual quota systems are illegal) or free points in a rating system, stripping the value and fairness of affirmative action.

The affirmative action aspect of the meritocracy is necessary because clearly not all individuals have similar resources. Not everyone has loving parents that are dedicated to teaching their children about the rigors of existence and giving them the tools, focus and guidance to become successful adults. Not everyone has parents with sufficient capital to provide resources and opportunities to significantly increase the probability of success. For example would someone like Taylor Swift really be the success she currently is at the moment if she was born to a single parent household where the guardian parent was working two minimum wage jobs just to get by? For such a circumstance it is highly unlikely that Miss. Swift would have become a successful entertainer instead being relegated to a waitress or service minimum wage job herself; note while Miss. Swift is talented at entertaining the fact that her parents had time to spend with her and large amounts of wealth to spend on her heavily tilted the scales of success in her favor.

People marvel at the rare exceptional cases of individual A becoming a successful… say neurosurgeon, despite growing up with an incarcerated father and an alcoholic mother or some similar hardship, but they conveniently fail to consider the vast majority of individuals who are unable to overcome such handicaps. It is completely inappropriate for society to chastise those that are unable to overcome hardships simply because a very select few are lucky enough to do so. Is it right to punish the 3rd generation for the sins, incompetence and/or bad luck of the 1st and/or 2nd generation? Therefore to create a genuine meritocracy, society must provide resources to eliminate the most crippling handicaps: everyone must receive sufficient shelter, food and an education otherwise society can never be a genuine meritocracy (it certainty is not one at present).

However, the original question was: can a meritocracy even come into existence in the first place based on the current structure and personality of society? There is a refrain that oddly rings of jealousy when rich individuals complain about the government providing food stamps for the poor when said rich individuals have the “great” burden of diverting a part of their $150,000+ a year salary to buy food. Taking the temperature of society it appears that most of the so-called “winners” forget that generational influence creates unequal starting positions instead believing that whether or not someone is successful is entirely of an individual’s making, a rationality that has been previously identified as foolish. Unfortunately this rationality is used to back a strong self-serving ego and will continuously provide a barrier to creating a genuine meritocracy.

It is difficult to understand the mindset that facilitates cries of “no fair” from individuals born into upper middle class or rich families towards individuals born into poor families who receive government assistance, but there seems to be one explanation that must be a part of the whole picture. Psychologically there are two perspectives that influence the concept of personal self-worth: absolute or relative. An absolute perspective of self-worth focuses on the individual in a vacuum and any judgment is applied along fixed concepts or values. A good example of this mindset is whether or not an individual believes scoring an 80% on a test in school is good (for some it is while for others it is not). A relative perspective of self-worth focuses on the individual when compared against other individuals and fixed concepts have far less importance in the evaluation. Returning to the above test example for a relative perspective an individual can score a 46% and still classify it as good if the class average was 33% even though 46% is by all accounts a failure on an absolute level.

Unfortunately it seems like too many people in society judge their self-worth on a relative level, a concept supported by the common refrain of “keeping up with the Joneses”; this mindset can create an underlying fear that providing assistance to individuals who are judged as “below” these relative thinking individuals could eventually lead to these assistance receivers surpassing the relative thinking individuals thus lowering their own self-worth all because the government had the audacity to help feed them. It is unclear what psychological aspects of the mind create a divergence between absolute self-worth and relative self-worth judgments, but one possibility is that those who judge on relative self-worth have little natural self-esteem and are scared of the truth about the limited significance of their actual character and accomplishments, thus they have to mitigate those limitations behind the failings of others. Sadly there does not appear to be any easy way of changing relative worth mindsets to absolute worth.

The meritocracy problem is not the only significant problem in a movement with a goal like OWS. Similar to almost everything in life, certainty or the probability of occurrence of the event is a critical element to whether or not someone will undertake a given action. However, certainty is especially important for group movements driven by ideas because of the tiered time elements. Most decisions have immediate or short-term time expirations like playing the lottery or criminal actions like shoplifting where all realistic possible outcomes from the decision making process are resolved shortly after the decision is made. For idea movements like the OWS continuous pressure must be applied by the proponents of the new idea in order to dethrone the existing idea beyond the new idea simply being a better idea because there are parties that benefit from the existing idea who would not benefit from the new idea. This pressure must continue even after acceptance of the new idea to ward off challenges from previously defeated inferior ideas or other new ideas that are not as beneficial to society. Therefore, proponents for societal ideas must be prepared to sacrifice over a long time period and even suffer multiple grievances, thus proponents must be even more committed.

Realizing the need for sacrifice societal movements need strong leaders that will inspire other individuals in the movement to make sacrifices. Some individuals believe that a hierarchical system utilizing leaders and followers is not appropriate, some even cite this feature as a strength of the OWS movement, but to hold this belief is to support a philosophy that will eternally have a low probability of accomplishing anything significant. As discussed above focus and commitment are important elements for successful movements and these elements are difficult to acquire if individuals are left to their own devices and expected to coordinate with each other to accomplish anything meaningful over a long period of time. The lack of a direct recognizable leadership hierarchy was one of the major reasons why the OWS movement collapsed, at least in the public eye, after it was removed from its initial base of operations.

What can a leader do to inspire individuals to fight for their common ideals? Despite what movies and television try to instill as quality leadership, simply giving a rousing inspirational speech is only useful in the short-term. When the consequences start hitting the fan non-zealous followers will quickly lose faith in leaders that only elect to orate from the sidelines. Such a characteristic is why President Obama is currently a poor leader. Instead the leader must act as a counterweight to the negative aspects of the consequences. One obvious means to neutralize this dissident element is for the leader to experience the sacrifices with the followers. The clear advantage of this strategy is that followers see that the leaders are also willing to sacrifice for the ideal building a greater level of trust. The disadvantage is that the scale of detriment rises with the magnitude of resistance.

For example some might argue that the detriment to the leader accepting similar consequence to the followers is that it is difficult to “lead” from a jail cell. However, looking over history no significant non-centralized power-based movement succeeded when the highest consequence was simply spending a few nights in jail. When the chief consequence is simply very short-term incarceration the opponents of the movement are not taking the movement seriously and realize that it has no real probability of success. However, when the opposition starts taking the movement seriously the consequences become more severe: longer jail terms, lawsuits, physical injury or even death, hence the real detriment. These results will lead to a difficult question: which is more damaging to the movement, leaders being maimed and killed or followers losing faith in their leaders? The answer is only something the particular movement can decide.

Instead of directly involving themselves in the consequence, leaders can alleviate or neutralize the consequence for their followers through effective legal arguments or counter negotiations with the third parties or the opposition party. One concern with this indirect strategy is that there are times when the opposing party begins to exert significant consequences and do not always allow for due process and other rights or in cases of movements outside the United States, such rights may not exist at all. Therefore, utilizing legal tactics to lessen or eliminate consequences may fail solely because the opposition does not allow them to succeed. Of course a leader could attempt to retain some credibility by blaming the failure of these avenues on opposition driven blockage.

Another issue for these types of movements in a democracy is that they must have the interests of the majority at heart. The “dark side” of democracy is that the majority is supposed to get what it wants, even if what it wants is wrong and/or foolish, and the minority is simply supposed to take it. This reality was not a large problem in the past for the minority because logical arguments could be made to break through and defeat inaccurate preconceived notions not backed by logic or evidence and convince members of the majority that a current idea was inferior to another idea. Unfortunately in the modern polarized global political system (which is not simply isolated to the United States) most people have developed the attitude that changing their opinion about anything is tantamount to complete failure so they resist change making it more difficult for the minority to induce change through dialogue. Fortunately for a movement like OWS the general goal of defeating income inequality is inherently favorable to the majority because it addresses a system where the minority can oppress the majority

Another way to associate goals of the movement to the will of the majority is the demonstration of belief both through altruism and accomplishment. As society has modernized it appears to have created a greater gap between what some would regard as the basics of humanity or human decency. Certainty there is a large outcry of assistance from strangers to strangers after natural disasters, but there is little caring or assistance during periods of normalcy. Therefore, a societal movement must demonstrate to bystanders that they should at least “root” for the success of the movement, if not join it themselves. Basically the general apathy and indifference that consumes people regarding the suffering of others must be defeated (i.e. I don’t care unless it is happening to me or someone directly associated with me). The accomplishment aspect bleeds into the certainty aspect in that people in the movement need to have the belief that they can actually win. Therefore, besides the overall goal of the movement sub-goals must be established that can be broadcast: recruitment goals, funding goals, opposition disruption goals, etc; some tangible metric that can be used by supporters to suggest that they are winning.

One of the trickier elements for a movement like OWS is their general goal when it comes to the distribution of power. Normally when a revolution type movement form the goal is to overthrow the current power structure and install one lead by the movement where individuals in the movement become the powerbrokers. In the case of OWS the presumed goal is to overthrow the current power structure and install a system where there is no guarantee that they will be powerbrokers, only allow for everyone to have a fair chance at becoming one. When thinking of it in a numerical sense in most revolutions the powerbrokers start at 10 and the revolutionaries at 1-2 and if the “rebels” win they go to 10 and the former powerbrokers go to 1-2. In the OWS situation the initial conditions are similar, but upon winning the “rebels” go to 5 and the former powerbrokers go to 4-6.

The chief problem with this change in the end result is that for most people in the movement the idea of acquiring power over the individuals/groups that will be disposed with a victory is a significant motivating factor, a reward for the sacrifices that are made to achieve victory. Such a mindset has played out numerous times in history with the oppressed overthrowing the oppressors and then becoming the oppressors themselves, especially against the former oppressors. Therefore, how much will members of a OWS like movement be willing to sacrifice for a seat at the table if that table will be open for everyone, especially if individuals who do not sacrifice receive the same general benefits? Ironically a leader of such a movement could motivate such sacrifice by tapping into the relative self-worth mindset by arguing that those who participate and sacrifice for the movement will enhance their legacies while those who don’t will be looked down upon even though the absolute tangible gains from the movement will be similar for all repressed parties.

The final issue is actually winning without centralized power or violence. The only genuine way to accomplish a victory in this situation is the effective use of numbers. Society has become dependent on an economic system that is a pyramid structure where a movement with numbers can simply collapse the entire system. Of course such a strategy relies on invoking Zappa’s philosophy of it being better to die on one’s feet than live on one’s knees. This ideal is important because for a movement without centralized power the highest probability of victory comes from a mutual assured destruction (MAD) strategy.

MAD works on two levels. First, it acts as a deterrent, as most know from the Cold War, neither side acts against the norm creating a stable, but stressed situation. Second, one party acts to trigger a response from the opponents significantly damaging, if not effectively eliminating, both sides. In the case for such a strategy with an OWS movement millions of individuals would simply need to stop working and buy only the bare minimum to survive. This reaction would create a self-catalyzing economic collapse that would erode the foundation of the global economy, especially if such action occurred in the United States. The powerbrokers would not be able to neutralize such an action and their “penthouse” positions would come crashing down along with the base, for despite some of the attitude possessed by the rich demographic if the base of the building collapses the penthouse will not “magically” remain aloft through levitation.

However, the crux of a MAD strategy, hence the clever and useful acronym, is who would be willing to destroy themselves in effort to induce certain changes? What typically prevents non-zealots from executing extreme actions: fear. Non-zealots fear that their sacrifices are not sufficient to accomplish the end goal, thus they are “throwing their life away” for no genuine progress. Therefore, to execute a MAD strategy one must eliminate this fear. Religious revolutionary leaders do so through promises of beneficial positions in the afterlife, i.e. defeat those heathens that hold Jerusalem and God will welcome you to heaven or blow yourself up to kill those Zionists and Allah will grant you virgins. An OWS movement really has zero religious zeal, despite the feelings of Jesus the Christ towards the poor (something forgotten by most rich people who claim to be Christian), so the most empirically relevant element for overcoming MAD trepidation is not available.

The magnitude of the sacrifice and movement have to be significant enough, so a few dedicated individuals who elect to bare the burden of sacrifice themselves as a flash/rallying point will simply result in needless sacrifice that will soon be forgotten. For example who remembers the names of the Tibetan monks that occasionally immolate themselves in the name of Tibetan independence? Interestingly there are millions of people that could be candidates for joining a movement that does not have a centralized power structure, thus will more than likely need to rely on MAD. Sadly their involvement could be regarded as controversial.

Those who are depressed have loosened their opinions of the value of life making them more amenable to taking risks and sacrifices with it for what could be viewed as a great purpose. In addition the relative self-worthy pendulum swings in the movement’s favor in that the depressed see little value in their lives so participating in such a magnifying movement may tap into their deflated ego. It must be noted that to some there would be clear moral pauses to incorporating individuals of such psychological states into such a movement in that will they simply be pawns as a means to an end? Also such incorporation could create a negative backlash against the movement whether justified or not. However, there is something to be said that depressed individuals are not mentally incompetent, thus they could freely decide whether or not to participate in a societal movement and what level of sacrifice they would be willing to devote to it.

Overall for a movement like OWS to succeed it requires one of three elements: 1) Numerous advocates in the current centralized power structure that will change the current system to be accommodate the goals of the movement; 2) Utilize violence to create an environment where the proposed goals of the movement provide less of a detriment to those in power than the detriment provided by the violence; 3) Execute a non-violent MAD strategy involving task and consumer elimination that threatens to collapse the entire economic system unless the demands of the movement are met. Some could argue that there is a fourth option in that millions could elect individuals to power in a democracy catalyzing the formation of option 1. However, this argument is difficult because the civil rights movement had a seasoned leader in LBJ with decades in government with time in both houses of Congress, an ability to effectively understand and play the political game and numerous friends, allies and even people just willing to listen; there is no such person with those characteristics with regards to income inequality and genuine meritocracy (Bernie Sanders does not have anywhere near the necessary clout). In the end unfortunately for OWS backers that particular movement elected to embark on a “none of the above” strategy, thus explaining why it has faded quickly and quietly into obscurity.

Is Curing Cancer the Appropriate Step? (Preparing for a World without Cancer)

Since 1971 when then President Nixon declared war on cancer society have awaited the breakthrough that would render the elimination of cancer as a societal and psychological boogie man. Interestingly the pursuit of this accomplishment has developed a certain type of viewpoint of how the future would operate after success with few individuals discussing how the world will change in both a positive and negative way. As counter-intuitive as it may seem would identifying a completely effective cancer treatment leave the world worse off than not identifying one at all?

At first thought almost everyone would find the above question preposterous citing both qualitative and quantitative rationalities for its ridiculousness. For example the National Institutes of Health (NIH) in 2008 estimated the annual costs of cancer to society were 201.5 billion (77.4 billion in direct medical costs and 124 billion in indirect mortality costs);1 those costs increased further in 2010 to $290 billion (154 billion in direct medical costs and 146 billion in indirect mortality costs).2 In 2007 cancer was responsible for approximately 13% of all human deaths globally (7.9 million)3 and in 2008 cancer killed another 7.6 million4 with overall occurrence rates increasing due to general increases in global life expectancies, changes in diets and lifestyles in the developing world, and changes to the environment. In addition there is the emotional damage that cancer afflicts against individuals who do not even have the condition (friends and family) that is not calculated in the mortality costs, regardless of whether or not the afflicted dies, raising economical and societal damage further.

Initially one may assume that the enormity of these numbers should dispel any individual arguing that a cure for cancer would be a bad thing, but the problem is that those numbers are only viewed through a positive lens not through a realistic lens. For example modeling economic costs associated with any condition or disease is currently simplistic and heavily dependent on certain assumptions. There are three common methods for estimating costs associated with various health conditions: Cost-of-illness (COI), Value of Lost Output (VLO) and value of statistical life (VSL).2

COI is the most common analysis method to calculate economic impact of an illness and assigned costs based on the sum of direct and indirect medical costs associated with the illness. Direct medical costs are sub-categorized as: diagnosis, drugs, hospital stays, surgeries, etc. Indirect mortality costs are sub-categorized as: transportation, income losses, pain and suffering reduced productivity, education, etc.5 Note that productivity losses (associated with indirect mortality costs) are typically modeled through the human capital approach, which calculates the potential production by an individual based on average wages adjusted for household productivity.5

The human capital approach is not the only method for calculating productivity, some analysis also use the friction cost method instead. Friction cost estimates the indirect costs of an illness relative to the amount of time it takes the employer/society to substitute the production lost from the individual who has taken ill.6 Basically costs are estimated by multiplying the number of days required for recovery by income and including an elasticity element for annual labor time versus labor productivity.6 Normally there is some form of time boundary (typically some number of days) associated with friction cost pertaining to the average expected recovery time for the illness. If recovery exceeds this boundary condition the excess costs are not counted towards the estimated production costs/losses. For example suppose person x contracts disease y that has an average recovery time of 30 days. If person x is not available to work for 17 days the productivity losses from all 17 days are counted. However, if person x takes 43 days only the first 30 are counted. This condition frequently results in lower estimated costs for a given disease because it typically does not encapsulate the more severe and costly cases of the disease.

COI also has two analysis “viewpoints”: prevalence or incidence. Prevalence estimates costs over a specific time period normally averaged to an annual cost, but does not focus on costs over the duration of the illness.5 Incidence estimates costs over the expected lifetime of an illness. Savings born from prevention strategies are derived from incidence-based analysis because of their timeline estimates over cross-sectional costs.5 While incidence estimates provide more information, they also require more assumptions and information, which can increase the probability for more inaccuracy in the results.

VLO estimates costs based on the impact on GDP with regards to lost capital, production, efficiency and other factors that affect commerce.2 VSL is categorized by two difference analysis methods: the human capital method and the mortality risk method.7,8 The human capital method calculates the present value of future income forgone due to death (similar to the method for COI). However, this method does not include intangible psychological elements on the family and friends of the deceased and ignores the non-working members of society who do not significantly act as human capital in the labor market.8 The mortality risk method calculates what costs members of society are willing to incur to change mortality risks from given illnesses. For example the World Bank classifies VSL as how people’s preferences affect the measurement of change (increase or decrease) in human well-being relative to the change in mortality risk based on the amount of money they would pay.9 Basically how much money would a person pay to reduce the chance of dying from disease A from 40% to 30%?

The reason these three methods exist is that they all examine economic costs relative to illness from different perspectives [public versus private (COI) or individual versus social (VOL) or some aspects of both (VSL) over different time periods]. However, because of these different analysis perspectives, along with complications due to co-morbidities, it is difficult to compare these methods directly.

Regardless of method calculating the possible savings from indirect costs is tricky. First of all productivity losses are more than likely overestimated because unlike past instances the current labor market functions on a shortage of jobs, not a shortage of labor. Of course some may argue against this point citing some of the higher paying jobs that have been vacant for years, but these jobs are highly specific demanding high education and experience levels, which are not available to a vast majority of the population, thus these jobs are radical outliers. Most modern vacant jobs are lower paying, but have high levels of competition including many individuals who are overqualified. Thus, most of the production from labor that is lost to cancer is more easily replaced now than in the past making the savings from curing cancer less than expected.

Another question is how the overall economy will be affected by the redirection of indirect cancer costs. For example current indirect cancer costs are high scale with a narrow focus (i.e. large amounts of money applied to a small section of the economy). If cancer is cured the indirect costs will be diverted more than likely at a smaller scale due to greater sector spread. Will this change in fund distribution result in a net gain or net loss for the economy? The loss of large-scale funds in the cancer treatment industry will result in job loss and contraction in this industry. The concern is that will the redirection of the funds be too scattered to significantly promote job growth in other fields, thus resulting in a negative economic impact? One counter-argument is that the new survivors will spend their money bolstering economic activity. While possible the real validity of this counter-argument is contingent on what happens to the assets owned by these individuals in probate and raises the question of whether government or private control of funds provides better stimulation to the economy.

Another concern is the increasing intracountry global inequality gap. While globalization has decreased the inequality gap between developed and developing countries, it has increased the inequality gap between rich and poor individuals within both developed and developing countries. Assuming that the general death total associated with cancer remains similar over the next 10 years as cited from 2007 figures above, then if a cure for cancer is discovered in 2015 over the next nine years 71.1 million people who should have died will live (and that does not include any offspring these individuals may have).

Note that the above estimate is probably on the low side because the World Health Organization (WHO) estimates that by 2030 at least 13.1 million worldwide will die from cancer.4 Based on the existing inequality level most of these survivors will not have vast amounts of wealth (this assumption makes sense because 70% of all cancer deaths in 2008 occurred in low- and middle-income countries),4 but instead will compete with other individuals for a pool of resources that is at best static and worst declining. This competition could place a greater strain on a vast majority of parties including those who developed cancer, but did not die, lowering the quality of life of a greater number of individuals.

Some may argue that while the savings born from indirect costs may be inaccurate and possibly non-existent, the savings from direct costs are certainly real and substantial. Direct cost savings are real, but more than likely will not be useful to society. The reason for this judgment is the commerce arrow that governs cancer treatment. When individual x develops cancer and receives treatment (note that second part) most of the time he/she has health insurance where after paying a deductible the insurance company will pay for a vast majority of the costs associated with the cancer treatment (80-100%, depending on the specifics of the plan). This payment will typically go to a hospital (most doctors do not own their own treatment centers, etc.). The hospital uses some of those funds to purchase elements of the treatment from various companies. Overall most of the costs associated with cancer treatment are born by the insurance companies, whether or not those costs are passed on to consumers is unclear, but is definitely a possibility.

If a cancer cure is developed, the direct costs of treating cancer will significantly drop reducing the amount of money that insurance companies pay to hospitals. Therefore, insurance companies will gain most of the savings from a cancer cure. However, the benefit to society from a standpoint of direct costs depends on what the insurance company does with these saved funds. There are ten common actions that a company can take with their earned profits:

1) Keep it on their balance sheet to pay for future expenses (i.e. suppose next year is not profitable);
2) Pay off existing debt;
3) Invest in new equipment or other modernization upgrades to increase production and/or lower costs;
4) Issue a dividend or increase the dividend to stockholders;
5) Hire more employees;
6) Increase wages and/or pay bonuses to various employees;
7) Buyback stock;
8) Invest in other companies either as a passive investment or a takeover;
9) Provide some benefit for the consumer (in the case of insurance this would most likely be reducing premiums);
10) Donate the money to a charitable cause;

There is little reason to suspect that insurance companies would pledge profit neutrality where insurance premiums would be lowered to correspond to the savings garnered by the cancer cure versus current cancer treatment. Whether legitimate or not the failure to lower premiums would be justified through arguing the prevalence of other chronic conditions like high blood pressure, obesity and high cholesterol. Anything else that could be done with the saved money that would benefit society directly or even indirectly like donating the money to charity, increasing stock dividends or hiring more employees seems even more far-fetched than lowering premiums.

With the most likely use of the saved funds going into the coffers of the insurance company to be used for CEO bonuses and other frivolous actions to bolster the already wealthy (modern reality dictates that this will happen) the newly saved direct cancer costs will not be reinvested into society at any real magnitude. Any rational person realizes that with decades of empirical evidence against it, supply side economics (a.k.a. trickle down) does not work thus increasing CEO bonuses is rather irrelevant to societal economic benefit. In addition other economic changes would lead various hospitals to lose millions of dollars (it stands to reason that they charge more for cancer treatments over the elements used in those treatments) and the medical companies that provide current cancer treatments will more than likely lose money as well because longer-term treatments yield more revenue than shorter-term treatments (which is what a cancer cure is assumed to be). Whether or not these losses will result in further expanded economic damage to society through things like a cutback in the existing workforce is unclear.

It is also important to address the fate of money devoted to researching a cancer cure. A vast majority of the money that funds cancer research comes from the government through the National Institute of Health (NIH), somewhere in the neighborhood of at least 5.6 billion.10 Therefore, it is reasonable to suggest that this money could be directed elsewhere from the NIH general fund to other worthy grant applicants. However, whether or not this will occur is unknown because of possible future cutbacks in NIH funds. For example some members of Congress may simply decide to eliminate a large amount of past cancer funding from the NIH in an inaccurate and foolish attempt to “cut government pork/waste”. While it is difficult for a legislator to cut funds for cancer research from a public relations standpoint, the public would not be so resistant to a cut in cancer funds that would have been redirected to say Chronic Fatigue Syndrome or something else.

The money derived from charitable organizations like the National Cancer Society is less likely to be recovered. Clearly the development of a cancer cure would heavily limit the continued functionality of such organizations. Most people who donate to cancer charities do so because of a personal connection to cancer, either they had it or know someone who has/had it. Therefore, it is unlikely that these individuals will donate to other charities if such a personal connection does not exist, they do not have a “charity donation quota” that needs to be met each year. Overall it stands to reason that most of the government funds for future cancer research will be directed to other medical research (unless Congress gets involved) and most of the private funds that would have gone to cancer research will not go towards other medical research. Some of these private funds could be invested in the economy yielding positive results, but the extent of benefit for such investment is unclear.

Part of the economic analysis associated with the possible societal influence of a cure for cancer is based on the assumptions that the cure would be widely available and will treat most, if not all, of the major forms of cancer. Initially it could be argued that the widely available assumption is not appropriate. However, the reasoning behind including this assumption is as followed. In the developed world it stands to reason that major insurance companies would cover the cost of the cure. This reasoning makes sense on two fronts: first, it is highly probable that a cure for cancer will cost less than the existing standard cancer treatment, thus it makes direct business sense for insurance companies that cover existing cancer treatments to shift coverage plans to cover the cancer cure.

Second, from a public perception standpoint any insurance company not providing coverage for a cancer cure would more than likely be basically ostracized from the marketplace with consumers avoiding that company in favor of one that does provide cancer cure coverage (recall that the assumption for this discussion is a cancer cure not a cancer vaccine thus people will still develop cancer). For the developing world it seems likely that various NGOs and charities will cover a majority of cancer cases with significant cost parameters.

So the general summary of change to society with the development of a cancer cure like treatment is as followed:

- Approximately 7.6 - 7.9 million people per year no longer die (assuming that the cure is available to all and that estimate may be on the lower end if cancer rates and deaths increase in the future which they are expected to);
- A vast majority of the direct costs associated with cancer treatment becomes increased profit for various insurance companies that will not result in an increased benefit to society;
- The growth/loss transfer to the general economy associated with indirect costs is unclear due to the simplistic level of modeling associated with cost replacement in the models themselves;
- The increased population will increase strain on existing resources, especially in developing countries, which have the majority of cancer deaths, as well as increase competition between individuals more than likely decreasing the quality of life of a larger number of individuals;
- There may be a contraction in employment at hospitals and other medical service companies, especially in high healthcare cost countries like the United States;
- Redirection of government grants and other monetary awards, both public and private, from cancer research to another medical condition/treatment should occur for government funds (again depending on how Congress acts), but not for private funds;

Understand that this blog post is not suggesting that the medical research community stop pursuing better cancer treatments, including one that may result in a cure, but instead is raising the important discussion point regarding how society may change in response to a cure. These changes are important to consider because of the momentous influence cancer as a physical disease and a psychological condition has on modern society. Cancer is in a rather unique position as a disease because while technically increasing age increases probability of development, no other disease permeates human health along all age groups at such a level of scale. Most other major diseases only afflict the elderly population. Therefore, eliminating this influence of cancer will cause significant change that must be accounted for and properly addressed to maximize the efficiency of curing cancer.

Overall it is troubling that no one really discusses these potential changes. Perhaps society is functioning under the belief that a cure to cancer is still decades away so addressing potential problems stemming from a cure is not necessary or that there will be no problems stemming from a cure. Neither of these explanations makes sense because there will be problems and even if a cure is delayed by decades developing a thought methodology to analyze how society could change is beneficial. Therefore, there are no excuses for the lack of attention being paid to possible negative societal changes that could be brought on by the development of a cure for cancer. As a starting point the most pressing issue for study is how the increased population will increase competition and possibly negatively influence society as a whole more so than if cancer is not cured.

Citations –

1. American Cancer Society. Cancer Facts & Figures 2012. Atlanta: American Cancer Society; 2012, page 1.

2. Bloom, D, et Al. “The Global Economic Burden of Non-communicable Diseases.” Harvard School of Public Health. World Economic Forum. 2011.

3. Wikipedia Entry – Cancer. 2013.

4. World Health Organization Fact Sheet N-297. Cancer. January 2013. In conjunction with Globocan 2008, IARC, 2010. http://www.who.int/mediacentre/factsheets/fs297/en/index.html

5. Corso, P, Soyemi, A, Lane, R. “Part II: Economic Impact Analysis. Cost of Illness.” Center for Disease Control and Heart Disease and Stroke Prevention.

6. Hutubessy, R, et Al. “Indirect costs of back pain in the Netherlands: a comparison of human capital method with the friction cost method.” Pain. 1999. 80:201-207.

7. Johansson, P. O. (2001). Is there a meaningful definition of the value of a statistical life? J Health Econ. 20(1):131-139.

8. Viscusi, W, and Aldy, J. “The Value of a Statistical Life: A Critical Review of Market Estimates Throughout the World.” Journal of Risk and Uncertainty. 2003. 27(1):5-76.

9. World Bank. “The Effects of Pollution on Health: The Economic Toll, in Pollution Prevention and Abatement Handbook, World Bank, Washington, DC. 1998.

10. National Institute of Health. Estimates of Funding for Various Research, Condition and Disease Categories (RCDC) between 2009 and 2014. April 2013. http://report.nih.gov/categorical_spending.aspx

Methane, Siberia and Bubbles

One of the more dynamic issues regarding the progression of global warming and its ability to induce detrimental effects on society is the role of methane trapped in permafrost on land and methane hydrates in the ocean and their release into the atmosphere as surface and ocean temperatures increase. Methane garners such attention because some are concerned that once a significant and consistent amount of methane starts to discharge from natural sources a runaway effect will begin dramatically increasing the probability of detrimental environmental damage. Unfortunately the estimates surrounding this “tipping point” vary considerably with large uncertainty because no one actually understand how the environment will respond once these methane sources start emitting methane.

While surface permafrost trapped methane is important because the ocean is absorbing most of the initial additional heat created by the combustion of fossil fuels the near-term focus should be placed there. Due to millions of years of methane accumulation1-3 and sea level change during the last glacial maximum it is known that large amounts of methane are trapped in hydrates (a form of methane in a clathrate molecule containing water ice) on or beneath the sea floor; however, the actual amounts in both quantity and stability are unknown (methane estimates range from 700 to 10,000 Pg of C).1,4-6 The stability may be unknown, but more frequent plumbs of methane release, especially around the Eastern Siberian Arctic Shelf (ESAS) have begun to worry scientists.7,8 The excessive greenhouse potential of large scale methane release should be a concern, thus it is important to determine a counter-strategy to reducing the probability that significant “tipping point” amounts of methane are released from these hydrates.

Typical hydrate formation was driven by pressure as melting temperatures for given compounds increase with pressure. Most of the hydrates that formed over time did so at large ocean depths (a few hundred meters below the sea floor) due to this melting temperature change principle.1 The ocean water column also experiences a reduction in temperature with an increase in pressure. Therefore, most methane hydrates are “protected” by a double security blanket: the higher melting point and the cooler deep ocean temperatures that are further buffered by a sediment layer. There are two types of methane hydrates deposits: stratigraphic and structural with a majority of the formations being stratigraphic, which appear to contain less methane than structural.9

The ESAS is especially important in the issue of methane release because its hydrates are located in much shallower water (45-50 meters) than most others because instead of relying on pressure to induce temperature changes for formation, the ESAS, as well as some other parts of the Arctic, simply used existing lower temperatures as a driver for hydrate formation.1,8 Unfortunately now with the Earth influenced by global warming these shallower hydrates have a much higher probability of releasing methane over their deeper counterparts. Also while some climate scientists have shown concern about the land based permafrost in Siberia, the average temperature of the ESAS bottom seawater is 12 – 17 degree C warmer than the average surface temperature over land based permafrost8,10,11 making methane release from the ocean more probable than release from the land.

Of course methane release from the hydrates is only the first step for producing additional atmospheric methane and aggravating global warming. There are additional “safeguards” even after methane bubbles have formed from the hydrates. First, the production of bubbles associated with melting attempts to destabilize the sediment column, but fortunately the depth of sediment packing prevents such a catastrophic occurrence typically limiting rate of release.12 Second, because the sediment column does not collapse it acts as a physical barrier and typically remains cold enough that the methane bubbles migrating through it results in the dispersion of the bubble.1 Third, free flowing sulfate creates a chemical barrier that can oxidize the methane.1 Fourth, methanotrophic bacteria can react with the methane converting the methane to CO2 (clearly not an ideal situation).

Not surprisingly though these “safeguard” are not able to neutralize all of the released methane. The probability of successful migration is largely dependent on bubble volume as the larger bubbles can create a larger pressure differential between both the sediment and the water versus the bubble at the top and bottom of the bubble.1,8,9 Unfortunately this critical element of bubble volume is difficult to measure or model; this is one of the elements that make it difficult to accurately portray methane release.

Despite the lack of good information pertaining to creating accurate models of methane hydrate release, there is little uncertainty that continued warming of the ocean by releasing larger concentrations of CO2 and other greenhouse gases into the atmosphere will result in large amounts of methane release from methane hydrates. One of the trickier elements for this situation is that CO2 mitigation is a long-term solution, but not a short-term solution and methane release may be an all-term problem. The reason for this concern is that while reducing CO2 emissions will eventually result in a cooling atmosphere, oceanic release of heat through convection should proceed at a much slower pace maintaining the threat of methane release for a considerable period of time after CO2 mitigation is completed. Therefore, a strategy for mitigating this release probability beyond mitigation of CO2 emissions must be developed.

CO2 emission reduction is a longer-term strategy even if it rapidly occurs because of the physics of ocean heating and cooling. The surface layer of the ocean is warmed by sunlight penetration typically increasing the ocean surface temperature beyond the above atmosphere leading to heat loss. This rate of heat transfer is determined by the temperature gradient of “cool skin layer”, a thin viscous region of the ocean (0.1 to 1 mm thickness) that is in contact with the atmosphere.13,14 Due to the heat transfer between the atmosphere and the cool skin layer water molecules are forced together in a more organized formation limiting heat transfer to conduction only. When dealing with the thermodynamics of conduction temperature gradients are critical.

Addition of excess greenhouse gases to the atmosphere trap heat and redirect random percentages of the heat back to Earth including the ocean surface. This heat only penetrates the “cool skin layer” warming the top portion of the layer changing the temperature gradient.13,14 The change decreases the gradient between the atmosphere and the top portion of the “cool skin layer” and increases the gradient between the top portion and bottom portion of the “cool skin layer”. Due to these gradient changes heat will travel between the top portion and the bottom portion of the “cool skin layer” reducing the probability that heat is expelled back into the atmosphere. Thus the greenhouse gases have to be eliminated (through technological or natural processes) after mitigation to allow the ocean-atmosphere gradient to normalize for the ocean to start expelling heat into the atmosphere on a consistent basis.

There are two general short-term strategies for reducing the probability of methane release into the atmosphere: prevent the methane hydrate from melting in the first place or prevent the methane from reaching the surface and entering the atmosphere after melting. Despite potential protests from certain parties, the execution of these strategies will entail technological techniques that can be regarded as geoengineering. Two strategies come to mind when attempting to prevent the hydrates from melting: cloud thickening and increasing ocean surface albedo. One important aspect of strategy selection is to focus on locality to limit the costs and increase efficiency of the strategy. Such a consideration handicaps the injection of sulfuric aerosols into the atmosphere to promote cooling because over a significant period of time (multiple years) it is nearly impossible to maintain localization of these aerosols due to wind currents, thus the aforementioned two options become the most attractive.

Fortunately because the late fall, winter and early spring temperatures in the ESAS provide no threat to inducing methane hydrate melting any executed strategy would only need to be administered at most five months per year (early May to early October). The chief advantages of cloud thickening is its easy execution utilizing wind-propelled ships with reactants that are not environmentally detrimental and in very limited testing seems to reduce atmospheric temperatures. The chief disadvantage of cloud thickening is that it is a catalytic agent in that it only thickens existing clouds; it cannot create clouds in clear skies. Therefore, while this catalytic element is not a significant problem when considering cloud thickening for a global solar radiation management strategy, it could be significantly detrimental in its inconsistency for a local strategy.

Increasing ocean surface albedo is a little trickier because there are two chief possibilities: increase ice coverage and increase wake formation. Increasing ice coverage is almost a non-starter because it would involve fighting against decades of additional absorbed oceanic heat that has been reducing Arctic ice coverage including in the ESAS. Therefore, the increased albedo must come from something else. One possibility is increasing wake formation. While the process of creating a wake is theoretically simple, propeller generated vortices pressurize air creating submerged bubbles that rise to the surface,15,16 its overall reliability is questionable. For example to create the necessary speed to produce wake from ships would be counterproductive due to negative elements associated with the fueling components of those ships (relying on wind would not be appropriate).

Therefore, instead of directly applying a wake, one can indirectly create a wake through the production of a surface bubble layer. Bubbles require little energy to create, thus the operational costs for such a system are low.17,18 Bubbles increase ocean surface albedo by increasing the reflective solar flux by providing voids that backscatter light.17 In addition modeling the reflective behavior of bubbles is similar to aerosol water drops because light backscattering is cross-sectional versus mass or volume dependent and the spherical voids in the water column have the same refractive index characteristics. Note that ocean surface albedo varies with angle of solar incidence. Common values are less than 0.05 at 12:00, below 0.1 at 65 degrees solar zenith angle and a maximum albedo, which range from 0.2 to 0.5, at solar zenith angle 84 degrees.19-22

Experiments have already demonstrated the creation of hydrosols from the expansion of air saturated water moving through vortex nozzles, which applies the appropriate level of shearing forces creating a swirling jet of water.18 Also by using an artificial two-phase flow smaller microbubbles can be created to the point of even creating interfacial films through ambient fluid pressure reduction.19 Microbubbles can possibly form these films because they typically last longer than visible whitecap bubbles, which rise and bust in seconds. Note that whitecaps are froth created from breaking waves and can increase ocean albedo up to 0.22 from the common 0.05-0.1 values.23

While whitecaps from waves and wakes do provide increased surface albedo, the effect is ephemeral. Microbubble lifespan can be influenced by local surfactant concentration and fortunately the ESAS has limited surfactant concentration that would influence this lifespan, thus granting more control in the process of creating those bubbles (less outside factors that could unduly influence bubble lifespan). For example, if these bubbles are created through technological means additional elements can be added to the reactant water like a silane surfactant that could add hours to the natural lifespan.24 Bubble lifespan is probably the most important characteristic for this form of ocean albedo increase.

Another method for creating microbubbles comes from biomedical engineering or biology arena where microfluidic procedures and sonication are used to enhance surfactant monolayers to stabilize microbubble formation.25 However, there are two common concerns about this method. First, it is used primarily in a laboratory largely for diagnostic and therapeutic applications, not in the field; therefore there may be questions about transition. Second, while sonication increases stabilizing time, it limits control of microbubble size distribution, which limits the total reflectiveness of the bubbles.26,27

An expanded and newer laboratory technique, electrohydrodynamic atomization, generates droplets of liquids and applies coaxial microbubbling to facilitate control over microbubble size. Unfortunately one concern with this technique is that as mentioned above ideal bubble size is in microns, this technique is currently only able to create single digit millimeter sized bubbles.25 However, the increased size may be offset by the increased stability of the bubble (less overall reflection, but longer residence times). Comparison testing will be required to make the appropriate judgment.

Initially the idea of cloud brightening was dismissed above due to its catalytic ability versus an inherent driving reactant ability, but this dismissal was based on cloud brightening as a standalone application in the ESAS. However, cloud brightening could be a useful secondary component to a microbubble system. Another point of note is that over time microbubble surface application will result in hastened cooling of the ocean, especially the surface, which should increase CO2 retention capacity. Basically increasing ocean albedo should result in a very small localized increase in CO2 absorption increasing ocean acidity.

Most of the above discussion has centered on preventing the hydrates from thawing versus preventing the released methane from reaching the atmosphere. The reason for this focus is quite obvious; preventing thawing is easier than preventing released methane from reaching the atmosphere, especially in the oceanic environment itself. There are two main methane “removal” reactions utilized by nature and neither one is appealing for eliminating ocean born methane.

The first and principle method of elimination involves the reaction of methane with a free hydroxyl radical (OH-) in the troposphere or stratosphere creating water vapor and CH3- radical. This CH3- radical usually later reacts with another hydroxyl radical to form formaldehyde. While this reaction almost exclusively occurs in the upper atmosphere transferring it to the ocean in some form will not improve upon the situation. Methane can also react with natural chlorine gas to produce chloromethane and hydrochloric acid (free radical halogenation), but this is another atmospheric reaction that probably cannot be effectively transferred to an ocean medium.

The chief ocean methane reaction involves metabolization by microorganisms known as methanotrophs (or methanophiles). There are two major types of methanotrophs (ribulose monophosphate users and serine carbon assimilators) divided into numerous additional groups, which use two principle reactions with selectivity governed by the availability of oxygen.28 Note that methanotrophs are also located in soils and landfills and aerobic/anaerobic methanotrophs are of different families.28 Both the aerobic and anaerobic basic reactions are shown below (the reactions have numerous intermediates and their efficiency is largely based on what type of monooxygenases (MMO) enzyme is utilized):28,29

CH4 + 2O2 → 2H2O + CO2 (1)

CH4 + SO4(2-) → HCO3- + HS- + H2O (2)

The aerobic reaction is the principle reaction between the two, but has two drawbacks. First, the consumption of oxygen limits its ability to scale and address large amounts of methane release from melting hydrates due to the creation of oxygen limiting factor regions (a.k.a. dead zones). However, this magnitude of this drawback is limited in the ESAS because of the limited amount of life by scale. Second, the reaction produces CO2 as a product, which may be a net detriment overall because of the lifespan of CO2 and increasing ocean acidity. Unfortunately this drawback is not as limited as the first because ocean mixing will de-localize the increase in acidity. The scaling efficiency of the anaerobic reaction is the chief problem with its use because most of the oceanic available SO4 is located near the ocean floor, which limits its usefulness once the methane release concentration begins to increase significantly. Therefore, it does not appear that either relying on existing methanotrophic or other methane-oxidizing bacteria or attempting to increase their numbers will be an effective strategy for addressing methane hydrate melting.

There is a bit of question whether or not methane in the ESAS is a genuine threat. Air sampling surveys have revealed large variability in methane concentrations versus the standard global background concentration of 1.85 ppm with average increases of 5-10%. Some have also calculated a total methane flux from the ESAS of 10.64 million tons of methane per year.30 However, modeling studies suggest that permafrost lags behind changes in surface temperature, thus current outgassing is tied to long-lasting warming initiated by permafrost submergence approximately 8000 years ago versus recent Arctic warming.31 Such a conclusion is possible, but the rationality seems far-fetched due to the magnitude of the time lag.

Overall the threat of significant methane release in the ESAS is a legitimate one, but not one that demands immediate strategy implementation. While immediate strategy implementation is not required, strategies to address this melting possibility must be studied to ensure a solid and effective plan when the time for implementation comes, which appears to be soon. Currently local production of microbubbles by some form of floating device (a buoy for example) initially appears to be the best strategy for preventing methane release, but as mentioned future study must be conducted to ensure the validity of this promise.

==
Works Cited

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2. Davie, M, and Buffett, B. “Anumerical model for the formation of gas hydrate below the seafloor.” J Geophys Res. 2001. 106:497–514.

3. Dickens, G. “Natural Gas Hydrates: Occurance, Distribution and Detection”
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7. Archer, D (2006): Destabilization of methane hydrates: a risk analysis. A Report Prepared for the German Advisory Council on Global Change (40pp). PDF

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