No matter how much you push the envelope, it will always be stationery.
… used to think that the brain was the most wonderful organ in my body. Then I realized who was telling me this.
— Emo Philips, comedian
Awareness … is the endpoint of a cascade of processing steps that occur below the surface. “By the time consciousness kicks in, most of the work has already been done.”
— John-Dylan Haynes***
There is a saying among women scientists who attend highly specialized engineering universities, where the girl-to-guy ratio is decidedly in their favor: “The odds are good, but the goods are odd.”
— Michio Kaku, in his book The Future of the Mind, pg. 143 (Doubleday, 2014)****
Thinking differently from others is therefore a prerequisite for creativity.
— (Power, 2015)
John-Dylan Haynes (*** see quote just above) is a scientist who studies decision making in the areas of the brain that process information without your conscious knowledge. In a fairly recent study, Dr. Haynes and his collaborators determined what areas of the brain were involved in making a decision by human subjects to press a button (Soon, 2008). The conscious motor decision took place after activity in other brain areas was detected. “The predictive information in the fMRI [functional magnetic resonance imaging] signals from this brain region [frontopolar cortex] was already present 7s before the subject’s motor decision. Taking into account the sluggishness of BOLD [blood oxygen level-dependent] responses, the predictive neural information will have preceded the conscious motor decision by up to 10s.” “Thus, there appears to be a double dissociation in the very early stages between brain regions shaping the specific outcome of the motor decision and brain regions determining the timing of a motor decision.”
“… it has been argued that the brain had already unconsciously made a decision to move even before the subject became aware of it (Soon, 2008).”
Indeed, as Dr. Haynes said. By the time consciousness kicks in, most of the work has already been done.”
Soon, Brass, Heinze, & Haynes. Unconscious determinants of free decisions in the human brain. Nature Neurosci. 11(5):543-5 (2008).
A very recent paper (Fang, 2016) examined the association between dietary magnesium and health. In this dose-response meta-analysis from 40 prospective cohort studies that included over one million (1,000,000) participants, the researchers found that, for each 100 mg/day increase in magnesium intake, the risk of stroke decreased by 7% (RR (relative risk):0.93; 95% CI (confidence interval):0.89-0.97, and was associated with a 10% lower risk of mortality. The highest category of magnesium intake, as compared to the lowest category, was found in the participants to reduce the risk of type 2 diabetes (RR: 0.74 (95% CI: 0.69-0.80).
“A dose-response analysis revealed that a 100 mg/day increase in dietary magnesium intake is significantly associated with a 7%, 22%, 19%, and 10% decrease in the risk of stroke, heart failure, type 2 diabetes, and all-cause mortality.” However, there was no clear association between magnesium and the risk of cardiovascular disease. In the U.S. and in Europe, the daily intake of magnesium does not generally meet the recommended amount. Epidemiological studies indicate that low levels of serum magnesium are associated with diseases such as chronic obstructive pulmonary disease (COPD), type 2 diabetes, and Alzheimer’s disease, among others (Fang, 2016).
We highly recommend taking supplemental magnesium. We take 400-600 mg per day of magnesium from our On Target Magnesium Plus.™
Fang et al. Dietary magnesium intake and the risk of cardiovascular disease, type 2 diabetes, and all-cause mortality: a dose-response meta-analysis of prospective cohort studies. BMC Med. 14:210 (2016)
Preliminary clinical studies are showing promising results in the treatment of pain in patients with sickle cell disease. Pain is the hallmark of sickle cell disease, with some patients in pain all of the time. Arginine has been found in these preliminary clinical studies to be effective against the pain due to vaso-occlusive blood clots. “Phase II clinical trials of arginine therapy for sickle-related pain are underway and a Phase III randomized controlled trial is anticipated in the near future (Bakshi, 2016).”
Sickle cell disease is described as an “arginine deficiency syndrome (Bakshi, 2016).” The “global arginine bioavailability ratio” (GABR) was developed to assess the state of arginine sufficiency as expressed in the ratio of arginine to arginine metabolites (ornithine and citrulline). The GABR is low, not only in sickle cell disease, but also in diabetes. Moreover, a low GABR “has been shown to be a strong predictor of cardiovascular disease and early mortality in general (Bakshi, 2016).”
Arginine can be found in our Inner Power,™ with each serving containing 6 grams of arginine. Suggested use is 1 to 3 servings a day on an empty stomach—at bedtime, upon awakening, or before exercise.
Bakshi and Morris. The role of the arginine metabolome in pain: implication for sickle cell disease. J Pain Res. 9:167-75 (2016).
The safest way to increase BAT (brown adipose tissue) thermogenesis is by exposure to cold (Yuan, 2017). Rutin is a dietary flavonoid shown, in a very recent study to increase energy expenditure like exposure to cold, “greatly increas[ing] core body temperature when animals were exposed to a cold environment (4 degrees C, 4 h) Genetically obese mice were able to switch energy sources from oxidizing glucose to oxidizing fat, a flexibility that is normally impaired in obese animals (Yuan, 2017).
In the study, genetically obese mice (Db/Db) and diet-induced obese mice (DIO) were treated with rutin (1 mg/ml added to their drinking water for 10 weeks). Increased thermogenesis in BAT was detected by the induction of “beige” tissue formation (in which WAT, white adipose tissue, is converted to a more BAT-like form, a process called “browning”), activating SIRT1/PPARgamma coactivator (PGC)-1alpha/mitochondrial transcription factor, increasing the number of mitochondria, and increasing UCP1 (uncoupling protein 1) activity. “Indeed, the expression levels of BAT markers, such as UCP1, Cidea, and Prdm16 were dramatically increased in BAT from rutin-treated DIO or Db/Db mice (Yuan, 2017).” These are changes that are seen in cold-exposed BAT. SIRT1 activation is particularly interesting as it has been associated with increased longevity in many studies.
Activated brown adipose tissue (BAT) has beneficial effects on lipid metabolism—for example, after cold exposure BAT “promotes the clearance of excessive triglycerides in the plasma by increasing lipid uptake into BAT,” where it is subsequently metabolized to create heat (thermogenesis) (Yuan, 2017).
Though certain FDA-approved drugs can promote the “browning” of white adipose tissue (WAT), they may be far more likely to have unwanted side effects than rutin—for example, rosiglitazone or beta-adrenergic agonist drugs (such as clenbuterol) have been reported to promote such “browning,” but are said not to be used in clinical practice for this purpose due to side effects.
The researchers (Yuan, 2017) conclude: “These findings reveal that rutin is a novel small molecule that activates BAT and may provide a novel therapeutic approach to the treatment of metabolic disorders.”
Each serving (2 capsules) of our AGEless™ contains 125 mg of rutin. This formulation was designed to protect against glycosylation (an aging mechanism in which glucose combines with proteins to form AGEs, advanced glycation endproducts). The prevention of AGE formation is another beneficial effect of rutin. We’ve been taking AGEless for umpteen years.
It is generally accepted that persistent infections (viral, bacterial, fungal, parasitical, etc.) can have serious effects on health by inducing hyperactivation of the immune system, such as by increasing the release of inflammatory cytokines. One such persistent infection is Helicobacter pylori (H. pylori), now well known for increasing the risk of ulcers and of gastrointestinal cancers (Herrera, 2009). The bacterium, believed to infect 40-50% of the world’s population, has been linked to many systemic diseases, including cardiovascular disease (Danesh, 1999) and cancer and some evidence suggests that it indirectly contributes to the development of Alzheimer’s disease. (Malaguarnera, 2004). In fact, a recent paper reports that H. pylori triggers double-strand breaks in DNA, which is consistent with its carcinogenic properties (Toller, 2011).
A presentation at a scientific meeting by M. Niehues and A. Hensel was reported in the journal Planta Medica (Niehues and Hensel. In vitro interaction of L-Dopa with bacterial adhesins [responsible for the adhesion of the bacterium to gastric epithelial cells] of Helicobacter pylori: an explanation for clinical differences in bioavailability?” Planta Medica 75:877-1094 (2009). The researchers here reported the surprising effect of H. pylori on the availability of L-Dopa taken by Parkinson’s disease patients. The L-Dopa became attached to bacterial adhesins from the H. pylori, leaving less unbound L-Dopa for actually treating Parkinson’s. The authors of the presentation suggest that this mechanism may explain why Parkinson’s patients infected with H. pylori do less well on a similar amount of L-Dopa as patients who are not infected with H. pylori.
Thus, Parkinson’s disease patients might benefit by eliminating or reducing H. pylori present in their systems. A dietary supplement available for this purpose that is both safe and effective (as well as inexpensive) is mastic, the gum resin of the mastic tree, Pistacia lentiscus L. Sandy takes Life Enhancement’s Bye-Lori Plus,™* which contains mastic, because Durk was infected with H. pylori for decades before eradicating it with antibiotics and Sandy wants to make sure she didn’t “catch” it from him.
HELICOBACTER PYLORI AND ARGININE
Pathogens such as Helicobacter pylori and Toxoplasma gondii defend themselves against their host’s immune system by producing arginases that limit nitric oxide (a powerful pathogen-killing substance) production by depleting L-arginine (Grohmann, 2010). Thus, increasing L-arginine might be another way to help eradicate Helicobacter pylori infections. We both take L-arginine (6-12 grams/day) in Inner Power Plus,™ available from Life Enhancement Products.
by Sandy Shaw
The difference between drug use and addiction or eating and metabolic diseases is time. The amount of time we take a potentially addictive drug determines whether we become addicted; this is also true for eating—eating for only a limited period of time can prevent the development of metabolic diseases, such as diabetes type 2 (Hatori, 2012).
An example of how time can determine the result of eating: a recent study of male mice fed a high fat diet found that restricting feeding to only eight hours a day WITHOUT REDUCING CALORIES as compared to being free to eat at any time prevented metabolic diseases (such as obesity, hyperinsulinemia, fatty liver, and inflammation).
Dopamine is required for the estimation of time by the internal clock. “Interval timing, the ability to discriminate durations in the seconds-to-minutes range, is a form of temporal cognition that requires an optimal level of dopaminergic function in cortico-striatal circuits in order to control time sharing and regulate clock speed.” A time interval is initiated by cortical oscillators in the ventral tegmental area of the brain by a burst of dopamine accompanied by a burst of theta power, which act as the “start gun” (Kononowicz, 2015).
The internal clock is critically controlled by dopaminergic agonists and antagonists. Dopamine agonists such as cocaine and methamphetamine (“speed”) have been shown to increase the speed of the internal clock, while dopamine antagonists such as haloperidol and raclopride have been shown to decrease the speed of the internal clock (Cheng, 2007).
In another study (Sysoeva, 2010), researchers found that there is an association of serotonin (5-HT) related genes with time perception. In their experiment, forty-four Russian Caucasian males (right handed and with a mean age of 22) compared two durations (they had to indicate which of them was shorter) on a computer monitor. “Many studies have reported an association between duration representation parameters and personality, specifically impulsivity and psychoticism.” Unsurprisingly, other studies have found psilocybin, a 5-HT (serotonin) receptor agonist, to affect time perception (Sysoeva, 2010).
“Despite the evidence … suggesting the centrality of DAergic [dopaminergic] modulation in mediating the drug-induced euphoria and timing distortions reported here, this explanation is likely an oversimplification of the processes underlying the individual differences observed in this study. Neuromodulators such as serotonin, GABA, glutamate, and norepinephrine, have also been found to influence time perception and to interact with DA [dopamine] in complex ways (Lake, 2013).” Another neurotransmitter with important effects on drug addiction and incentive-motivated behaviors is acetylcholine (Lester, 2010).
WHEN TIME SLOWS DOWN
You’ve all experienced it—the times when sudden danger appears, such as your car is about to hit a tree, and time slows release of adrenaline as you rapidly close in on the tree. As explained above, stimulants such as methamphetamine cause a large release of dopamine and this increases the speed of the internal clock. A hypothesis proposes that the reason this feels like time is slowing down is that your brain sees time as the amount of information it processes—the more bits of information is counted as a longer period of time compared to the usual number of bits you experience as “regular” time (Eagleman, 2005).
In a similar fashion, seeing an event in “slow motion” causes observers to believe that more time had passed than actually had (Caruso, 2016). Thus, time is underestimated.
A very recent paper (Soares, 2016) reported how mice judged the passage of time (judging the duration of intervals). Using a pharmacogenetic method to suppress dopaminergic neuronal activity in the substantia nigra pars compacta, they found that “[s]ituations in which DAergic [dopaminergic] activity is elevated naturally, such as states of high approach motivation, response uncertainty, or cognitive engagement are associated with underestimation of time. Conversely, situations that decrease DAergic activity, such as when fearful or aversive stimuli are presented are associated with overestimation of time.”
The bottom line: “… pleasurable events boost dopamine release, which should cause your internal clock to run faster … so that short intervals seem longer than they are (Simen, 2016).”
Time stands still if you go fast enough.
—Stephen F. Kaufman, marial arts professional (Ch.
19 in his book “The Way Of The Modern Warrior”)
Who hasn’t experienced FLOW? The trick is being able to produce it when you want it.
Flow is often described as a state of effortless concentration so deep that people who experience it lose their sense of time. It gives you a sense of acting without conscious awareness, of time slowing down, of perceiving yourself to be moving through a dreamlike state.*
We knew a highly skilled champion racecar driver (Mickey Thompson) who told us that using a BLAST family formulation of ours had, in a very long off-road auto race (the BAJA 1000, when it was 1000 miles rather than 1000 kilometers) resulted in time slowing down, with everything happening exactly right and without any conscious effort on his part. He said that it felt like the flow he had experienced in his best races. The formulation that Mickey took was one of those we designed for our own use that contains the amino acid phenylalanine. Phenylalanine can be converted into tyrosine (which is then converted to dopamine) but also into phenethylamine (also called phenylethylamine), a neuromodulator that provides mental energy like caffeine, but also acts as a stimulus barrier (helps to filter out distractions). Phenylalanine is found in our BLAST formulas.
Caffeine provides mental energy in a different way than phenylalanine (see above). Phenylalanine is a natural compound that increases dopamine (via conversion to tyrosine) but, unlike caffeine (a xenobiotic), it does not mimic the effects of amphetamine and cocaine, like caffeine can do at 4-5 times the average human consumption of coffee. At high doses (300-800 mg), caffeine can increase feelings of anxiety, nervousness, and insomnia. Caffeine does NOT have addictive potential at the usual level of human consumption (50-300 mg or 1-3 cups of coffee), but induces feelings of well-being, alertness, energy, and ability to concentrate. Most of the effects of caffeine are reported to take place at adenosine receptors, where caffeine is an inhibitor (Nehlig, 2000). There are other changes, though, which include a 26-30% increase in the densities of cortical muscarinic and nicotinic cholinergic receptors; the evidence supports significant alterations in adenosine, adrenergic, serotonergic cholinergic, and GABAergic systems (Shi, 1993).
NUTRIENTS THAT MODIFY THE SPEED OF THE INTERNAL CLOCK
The amino acid tyrosine is precursor to dopamine, that is, converted to dopamine. (The amino acid phenylalanine is converted to tyrosine, so it is an indirect precursor to dopamine.) As noted above, dopamine agonists increase the speed of the internal clock (Cheng, 2007; Meck, 1987). This feels like time is slowing down. (Interestingly, “flow” is a process in which time does feel as though it is slowing down.)
WHEN PLEASURE BECOMES A HABIT
In the scientific literature, addiction is often called habit formation. Habit formation differs immensely from goal-directed activity. Where goal-directed activity is influenced by the outcome of performing an action, addictive activity is not—a negative outcome does not influence it.** If an action is habitual, “then devaluation should have no effect on performance, since habits are elicited by antecedent stimuli which are not affected by devaluation. “… habitual behavior is not controlled by the action-outcome contingency … (Yu. 2009)”
This can be seen in lever pressing by experimental animals. “At first lever pressing is goal-directed and sensitive to manipulation like outcome devaluation. Under certain conditions, it can become more habitual and impervious to changes in the value of the outcome … Studies in flies, mice, rats, horses, monkeys, and humans have shown some version of this transition from more flexible and goal-directed behavior to inflexible and habitual behavior.” (Yu, 2009)
It was purely the feeling that had captivated me, made me sacrifice everything to it, gladly, joyfully. It was a seashell’s pristine whisper in my ear, warm sun rising in my heart, fireflies winking in the nerves.
—Will Bohnaker, Haunts of The Aardwolf, on the allure of caffeine
EATING: DELAY DISCOUNTING
A recent paper (Johnson, 2010) points to a proposal that “deficits in reward processing may be an important risk factor for the development of obesity, and that obese individuals may compulsively consume palatable food to compensate for reward hyposensitivity.” This is another way of saying “self-medication.”
The dopaminergic nervous system is critically involved in the perception of pleasure from eating and sex. In fact, “the degree of pleasure from eating correlates with [the] amount of dopamine release (Stice, 2008).” The chronic overeating of high fat and high sugar foods causes a decrease in the sensitivity of dopaminergic neurons as a result of downregulation (reduced signaling). Animal studies have found similar effects from overeating and also in response to chronic drug use. Both overeating and the use of addictive drugs cause downregulation of dopamine D2 receptors and decreased D2 sensitivity.
A deficiency in the release of dopamine in the dorsal striatum may also be seen in individuals with a certain variant (allele) of the D2 dopaminergic receptor gene, the Taq1A A1 allele; it is interesting to note that this allele is involved in impulsivity, which is defined as “the relative preference for a smaller reward, sooner in time, compared to a larger reward, later in time … (Eisenberg, 2007)” This is called delay discounting—and “non-human research suggests that corticostriatal mesolimic substrates mediate delay discounting performance and that dopamine is the critical neurotransmitter involved.” (Eisenberg, 2007) The famous marshmallow experiments were a particularly notable example of delay discounting.
MONOAMINE OXIDASE A (MAOA) AND IMPULSIVITY
Monoamine oxidase A (MAOA) is a gene importantly affecting impulsivity. “… the risk imparted by the specific genetic variation studied here [MAOA] contributes to the impulsive dimension of this complex behavior [aggression].” The monoamine oxidase A (MAOA) gene, is of two types—MAOA-L (the low expression variant) and MAOA-H (the high expression variant). MAOA-L is associated with an increased risk of violent behavior. “Arguably, the clearest link between genetic variation and aggression exists for monoamine oxidase A (MAO-A) … a key enzyme in the catabolism [breakdown] of monoamines, especially serotonin.” The enzyme catabolizes dopamine, serotonin, and norepinephrine, reducing their availability for signaling at neuronal synapses (Meyer-Lindenberg, 2006). Hence, reduced catabolism, as with the MAOA-L variant, will not decrease the availability of dopamine, serotonin, and norepinephrine for signaling as much as the MAOA-H variant.
Goal-directed dimensions of aggression have been associated with psychopathy, often accompanied by diminished empathy and remorse. In their study (Meyer-Lindenberg, 2006), the researchers found that “men, but not women, carrying the low-expression MAOA genotype showed increased [emotional] reactivity during retrieval of negatively valenced emotional material.” Interestingly, men have only one allele (copy) of the MAOA gene, whereas women have two. The reason for this is that men have only one X chromosome (where the MAOA gene is located), while (of course) women have two. Interestingly, estrogens have been shown to affect the expression of MAOA in the brain (Meyer-Lindenberg, 2006).
Higher dominance has been associated with the low expression variant of MAOA (MAOA-L) and aggression in males in studies of primates.
SEROTONIN AND IMPULSIVITY
As noted above, serotonin deficiency is associated with impulsive behavior. This can be corrected by taking tryptophan, the amino acid that is converted to 5-hydroxytryptophan by the enzyme tryptophan hydroxylase and then to serotonin. However, some individuals are unable to make this conversion in sufficient amounts because their version of the enzyme lacks adequate potency. A way to overcome this is to take 5-HTP (5-hydroxytryptophan), which bypasses the need for tryptophan hydroxylase. We suggest taking 25 to 50 mg of 5-HTP at bedtime. We get ours from our Serene Tranquility with 5-HTP.™
DELAY DISCOUNTING MEETS THE GRASSHOPPER AND THE ANT
Another experiment on delay discounting (like the marshmallow experiments) was performed in human subjects, who made a series of choices between early and delayed monetary rewards while they were examined by fMRI (functional magnetic resonance imaging) (McClure, 2004). As a result, the researchers developed a hypothesis for how the brain decides between the early and later rewards. “… we hypothesize that short-run impatience is driven by the limbic system, which responds preferentially to immediate rewards and is less sensitive to the value of future rewards, whereas long-run patience is mediated by the lateral prefrontal cortex and associated structures, which are able to evaluate trade-offs between abstract rewards, including rewards in the more distant future.” They allude to the metaphor of the grasshopper and the ant. The grasshopper spends its time enjoying the present and ignoring what may come later, while the patient ant works diligently preparing for the future. The authors call delay discounting the competition between the “impetuous limbic grasshopper” and the “provident prefrontal ant.” (McClure, 2004).”
In sum, the researchers suggest that “human behavior is often governed by a competition between lower level, automatic processes that may reflect evolutionary adaptations in particular environments, and the more recently evolved, uniquely human capacity for abstract, domain-general reasoning and future planning.”
Another hypothesis on the neurochemistry of delay discounting (Kravitz, 2012) proposes that addiction (in which the future consequences of using drugs are ignored) depends upon the interaction between dopamine D1 receptors and dopamine D2 receptors: dopamine D2 receptors counteract dopamine D1 receptors in determining the probability of performing a future action. The D1 receptors induce persistent reinforcement, while the D2 receptors induce transient “punishment” (negative signaling) for the performance of a future action. “In contrast, depression is marked by impaired reinforcement from positive stimuli and heightened punishment from negative stimuli (Kravitz, 2012).”
SPEAKING OF ANTS …
Yes, speaking of ants, a recent paper appeared in the “Research Highlights” section of the 29 Sept. 2016 Nature which reported that ants can get hooked on morphine. The ants were given access to sugar water laced with morphine. Then, over the course of several days, the amount of sugar in the water was reduced while the morphine content was increased, until eventually there was NO sugar in the water, only morphine. The ants, given a choice between sugar water and the sugar-free morphine solution, preferred the sugar-free morphine by 65% to 35%. Plus the ants’ brains showed elevated levels of dopamine, just as addicted mammals do. The authors were said to suggest that ants might make a good model for studying addiction in humans. Durk wonders why 35% of the ants DIDN’T choose morphine … Sandy suggests that maybe those ants had a different version of the D2 dopamine receptor.
HIGH IMPULSIVITY PREDICTS THE SWITCH TO COMPULSIVE COCAINE-TAKING
Rats, like humans, can get addicted to drugs. When rats are exposed to cocaine, 15-20% of them become addicted, which is similar to that observed in humans (Belin, 2008).
“… the essential feature of addiction … [is] … the persistence of drug-seeking in the face of negative consequences …” explain researchers in a 2008 paper (Belin, 2008). In their study, they found that high impulsivity “predicts the development of addiction-like behavior in rats … [and they note that, in humans,] … there is a high comorbidity between drug addiction and disorders characterized by impulsive behavior, such as attention deficit-hyperactivity disorder.”
Low serotonin levels are thought to be a cause of impulsivity. For example, reducing serotonin levels by tryptophan-restricted diets results in more impulsive choices in experiments. A recent paper (Bevilacqua, 2010) found that a mutation in the serotonin 2B receptor predisposed a Finnish population to severe impulsivity.
Lithium may reduce impulsivity, but studies reporting this association have involved doses much higher than the low-dose form that we use. One such study (in rats) found that a “moderate” dose of lithium (20 mg/kg) suppressed impulsive behavior (Ohmura, 2012). Research involving the low concentrations of lithium found in mineral waters and in some tap water has reported reduced impulsiveness and suicide in people.
Another way to reduce impulsivity is to take tryptophan (precursor to serotonin). See above in “Eating: Delay Discounting.”
Whatever you may think of Mr. Trump, he has revolutionized the way this government functions. This is not just the election of a “new” president, but the initiation of a truly new way to govern where each individual has a voice, where each man or woman can speak directly to the president, something that has NEVER before been possible.
Trump uses social networking, something no president has done before. In so doing, his “tweets” can be answered by anyone. The bureaucracy and the mainstream media are both bypassed.
A post (Feb. 2, 2017) by John Robb at Global Guerillas puts it this way, “National governance isn’t just in Washington [DC] anymore. It’s  conducted everywhere at once. Everyone, from the government bureaucrat to the corporate executive to the owner of a Twitter account is now an active participant. It is now MUCH more participatory than it has EVER been. (emphasis on MUCH added).”
The post continues, “Bureaucratic governance mass media coverage focuses on one problem at a time (serially) … In contrast, networked governance can focus on many [problems] in parallel. This makes it very difficult for gatekeepers to exercise control.”
This is how Mr. Trump is flummoxing the media and his political enemies: he tweets and he distracts them from other, more important issues. They can’t respond to everything at once and he has sent them off in directions of his choice to keep them busy.
In a second post (Feb. 10, 2017), at Global Guerrillas, John Robb adds to his well-done analysis of the merging of social networking and politics. He sees social networking as containing three political networks: insurgency, orthodoxy, and participatory. The insurgency is the way that Trump became president without much advertising—about 10% of Hillary’s—and despite the opposition of most of the press. Trump was the catalyst here.
The orthodoxy “arose out of the ashes of the political parties and it is growing without any formal leadership (from the Feb. 10, 2017 post).” It is the part of social networking that fiercely opposes Trump. “Trump feeds the outrage that fuels it,” says Mr. Robb.
The participatory group is something of a combination of the insurgency and the orthodoxy.
In a recent article (Egerstedt, 2011), the author commented on a paper (Liu, 2011) about social networking, specifically, how they can be controlled. The conclusion was that they are VERY difficult to control. “… both social networks and naturally occurring networks, such as those involving gene regulation, are surprisingly hard to control.” (Egerstedt, 2011)
The article contained an analysis of how you choose the most influential individuals (the driver nodes). “The nodes are individual decision makers … The edges [the connections] are the means by which information flows and is shared between nodes.” The analysis continues: “… driver nodes tend to avoid the network hubs. In other words, centrally located nodes are not necessarily the best ones for influencing a network’s performance … the most influential members may not be those with the most friends.” What I think this means is that the most influential decision makers may not be “joiners.” They are influential because of their ideas, which can be reached by large numbers of others without these influential people having any knowledge of who these “others” are.
A social network is a very different form of social connection, because it is not necessary to actually KNOW anybody. You can be a hermit living on a mountain top nowhere near anybody else and still be as connected to the network as “people who need people.” Something like 24,000,000 people are following Trump at Twitter, but few are actually likely to know him or to “need” him.