Home » 2013 » July (Page 2)

Monthly Archives: July 2013

Advertisements

Obesity, Metabolic Disease and Pathways to a Cure

What follows is my abridged version of one of the most significant summaries of research into diet and human health.  This article was written by Moises Velasquez-Manoff  for Mother Jones in April of 2013. When you go to the full text of this article you will also find a video and other helpful information.  The focus of this abridgement is to present the key advances in our understanding of diet, obesity and metabolic syndrome.  Omitted are the implications and recommendations with respect to dietary changes. I would recommend that you read the full article at Mother Jones. The URL Web address is below.

Are Happy Gut Bacteria Key to Weight Loss?

by Moises Velasquez-Manoff

[Abridged version for readers of DataDrivenViewPoints.com]

MOTHER JONES – April 22, 2013

http://m.motherjones.com/environment/2013/04/gut-microbiome-bacteria-weight-loss

Highest-Calorie-Foods

In 2004 a curious diabetes specialist in Buffalo, New York, named Dr. Paresh Dandona, fed nine normal-weight volunteers an egg sandwich with cheese and ham, a sausage muffin sandwich, and two hash brown patties to see what effect this had on their bodies.

He found that levels of a C-reactive protein, an indicator of systemic inflammation, shot up “within literally minutes,” and remained elevated for hours. Inflammation is a natural and important part of our immune system response, but inflammation can also cause collateral damage, especially when the response is overwhelming—like in septic shock—or when it goes on too long.

Chronic, low-grade inflammation has long been recognized as a feature of metabolic syndrome, a cluster of dysfunctions that tends to precede full-blown diabetes and that also increases the risk of heart disease, stroke, certain cancers, and even dementia—the top killers of the developed world. The syndrome includes a combination of elevated blood sugar and high blood pressure, low “good” cholesterol, and an abdominal cavity filled with fat, often indicated by a “beer belly.” Could chronic systemic inflammation (CSI), in fact, be a major cause of metabolic syndrome disorder? A fast-food breakfast inflamed, he found, but a high-fiber breakfast with lots of fruit did not. A breakthrough came in 2007 when he discovered that while sugar water, a stand-in for soda, caused inflammation, orange juice—even though it contains plenty of sugar—didn’t.

This time, along with their two-sandwich, two-hash-brown, 910-calorie breakfast, one-third of his volunteers—10 in total—quaffed a glass of fresh OJ. The non-juice drinkers, half of whom drank sugar water, and the other half plain water, had the expected response—inflammation and elevated blood sugar. But the OJ drinkers had neither elevated blood sugar nor inflammation. The juice seemed to shield their metabolism. “It just switched off the whole damn thing,” Dandona says. Other scientists have since confirmed that OJ has a strong anti-inflammatory effect.

What caught Dandona’s attention was increased blood levels of a substance called endotoxin. This molecule comes from the outer walls of certain bacteria. If endotoxin levels rise, our immune system perceives a threat and responds with inflammation. Where had the endotoxin come from? We all carry a few pounds’ worth of microbes in our gut, a complex ecosystem collectively called the microbiota. The endotoxin, Dandona suspected, originated in this native colony of microbes. Somehow, a greasy meal full of refined carbohydrates ushered it from the gut, where it was always present but didn’t necessarily cause harm, into the bloodstream, where it did. But orange juice stopped that translocation cold.

If what some scientists now suspect about the interplay of food and intestinal microbes pans out, it could revolutionize the $66 billion weight loss industry—and help control the soaring $2.7 trillion we spend on health care yearly. “What matters is not how much you eat,” Dandona says, “but what you eat.”

Scientists now suspect that our microbial communities contribute to a number of diseases, from allergic disorders like asthma and hay fever, to inflammatory conditions like Crohn’s disease, to cancer, heart disease, and obesity. As newborns, we encounter our first microbes as we pass through the birth canal. Until that moment, we are 100 percent human. Thereafter, we are, numerically speaking, 10 percent human, and 90 percent microbe. Our microbiome contains at least 150 times more genes, collectively, than our human genome.

The importance of intestinal microbes to our health has grown increasingly evident. Animals raised without microbes essentially lack a functioning immune system. Entire repertoires of white blood cells remain dormant; their intestines don’t develop the proper creases and crypts; their hearts are shrunken; genes in the brain that should be in the “off” position remain stuck “on.” Without their microbes, animals aren’t really “normal.”

Scientists now suspect that our microbial communities contribute to a number of human diseases, from allergic disorders like asthma and hay fever, to inflammatory conditions like Crohn’s disease, to cancer, heart disease, and obesity. As newborns, we encounter our first microbes as we pass through the birth canal. Until that moment, we are 100 percent human. Thereafter, we are, numerically speaking, 10 percent human, and 90 percent microbe. Our microbiome contains at least 150 times more genes, collectively, than our human genome. Sometime in childhood, the bustling community of between 500 and 1,000 species stabilizes.

Our stool is roughly half living bacteria by weight. Every day, food goes in one end and microbes come out the other. The human gut is roughly 26 feet in length. Hammered flat, it would have a surface area of a tennis court. Seventy percent of our immune activity occurs there. The gut has its own nervous system; it contains as many neurons as the spinal cord. About 95 percent of the body’s serotonin, a neurotransmitter usually discussed in the context of depression, is produced in the gut. So the gut isn’t just where we absorb nutrients. It’s also an immune hub and a second brain. And it’s crawling with microbes. They don’t often cross the walls of the intestines into the blood stream, but they nevertheless change how the immune, endocrine, and nervous systems all work on the other side of the intestine wall.

Science doesn’t know exactly what goes wrong with our microbes in disease situations but a loss of intentional microbe diversity appears to correlate with the emergence of illness. Children in the developing world have many more types of microbes than kids in Europe or North America yet develop have fewer allergies and less asthma. In the developed world, children raised in microbially rich environments—with pets, on farms, or attending day care—have a lower risk of allergic disease.

Some studies find that babies born by C-section, deprived of their mother’s vaginal microbes at birth, have a higher risk of celiac disease, Type 1 diabetes, and obesity. Early-life use of antibiotics—which tear through our microbial ecosystems like a forest fire—has also been linked to allergic disease, inflammatory bowel disease, and obesity. Those who study human microbial communities fret that they are undergoing an extinction crisis.

If our microbiota plays a role in keeping us healthy, then how about attacking disease by treating the microbiota? After all, our community of microbes is quite plastic. New members can arrive and take up residence. Old members can get flushed out. Member ratios can shift. So the microbiota represents a huge potential leverage point in our quest to treat, and prevent, chronic disease. In particular, the “forgotten organ,” as some call the microbiota, may hold the key to addressing our single greatest health threat: obesity.

One-third of Americans are now considered overweight, and another third obese. Worldwide, one-fourth of humanity is too heavy, according to the World Health Organization. One-third of Americans are now considered overweight, and another third obese. Worldwide, one-fourth of humanity is too heavy, according to the World Health Organization.

The long-dominant explanation is simply that too little exercise and too many calories equals too much stored fat. The solution: more exercise and a lot more willpower. But there’s a problem with this theory: In the developed world, most of us consume more calories than we really need, but we don’t gain weight proportionally. If you run a daily surplus of just 500 calories you should gain a pound of fat per week, but we either gain weight much more slowly, or don’t gain weight at all.

Some corpulent people, meanwhile, have metabolisms that work fine. Their insulin and blood sugar levels are within normal range. Their livers are healthy, not marbled with fat. And some thin people have metabolic syndrome, often signaled by a beer gut. They suffer from fatty liver, insulin resistance, elevated blood sugar, high blood pressure, and low-grade, systemic inflammation. From a public health perspective, these symptoms are where the real problem lies—not necessarily how well we fit into our jeans.

In one study, mice raised without any intestinal microbes could gorge on food without developing metabolic syndrome or growing obese. But when colonized with their native microbes, these mice quickly became insulin resistant and grew fat, all while eating less food. Another researcher suspected that low-level inflammation might be the cause for this. To prove the principle, he gave mice a low dose of endotoxin, that molecule that resides in the outer walls of certain bacteria. The mice’s livers became insulin resistant; the mice became obese and developed diabetes. A high-fat diet alone produced the same result: Endotoxin leaked into circulation; inflammation took hold; the mice grew fat and diabetic. Then came the bombshell. The mere addition of soluble plant fibers called oligosaccharides, found in things like bananas, garlic, and asparagus, prevented the entire cascade—no endotoxin, no inflammation, and no diabetes. Oligosaccharides are one form of what’s known as a “prebiotic”.

Cani had essentially arrived at the same place as Dandona with his freshly squeezed orange juice. Junk food caused nasty microbes to bloom, and friendly bugs to decline. Permeability of the gut also increased, meaning that microbial byproducts—like that endotoxin—could more easily leak into circulation and spur inflammation. Simply adding prebiotics—in this case, Bifidobacteria—kept the gut tightly sealed, preventing the entire cascade. Our sweet and greasy diet changes gut permeability and alters the makeup of our microbial organ. Our “friendly” community of microbes becomes pathogenic, leaking noxious byproducts where they don’t belong.

Probiotics are bacteria thought to be beneficial to digestion, like the lactobacilli and other bacteria in some yogurts. In the future probiotics might be bacteria derived from those found in Amazonian Indians, rural Africans, even the Amish—people, in other words, who retain a microbial diversity that the rest of us may have lost.

Ultimately, the strongest evidence to support microbial involvement in obesity may come from a procedure that, on the face of it, has nothing to do with microbes: gastric bypass surgery. The surgery, which involves creating a detour around the stomach, is the most effective intervention for morbid obesity—far more effective than dieting.

Originally, scientists thought it worked by limiting food consumption. But it’s increasingly obvious that’s not how the procedure works. The surgery somehow changes expression of thousands of genes in organs throughout the body, resetting the entire metabolism. In March, Lee Kaplan, director of the Massachusetts General Hospital Weight Center in Boston, published a study in Science Translational Medicine showing a substantial microbial contribution to that resetting.

He began with three sets obese mice, all on a high-fat diet. The first set received a sham operation—an incision in the intestine that didn’t really change much, but was meant to control for the possibility that trauma alone could cause weight loss. These mice then resumed their high fat diet. A second set also received a sham operation, but was put on a calorically restricted diet. The third group received gastric bypass surgery, but was then allowed to eat as it pleased. As expected, both the bypass mice and dieted mice lost weight. But only the bypass mice showed normalization of insulin and glucose levels. Without that normalization, says Kaplan, mice and people alike inevitably regain lost weight.

To test the microbial contribution to these outcomes, Kaplan transplanted the microbiota from each set to germ-free mice. Only rodents colonized with microbes from the bypass mice lost weight, while actually eating more than mice colonized with microbes from the other groups. In humans, some studies show a rebound of anti-inflammatory bacteria after gastric-bypass surgery. Dandona has also noted a decline in circulating endotoxin after the procedure. If we understand the mechanism by which the microbiota shifts, he says, perhaps we can induce the changes without surgery.

NOT EVERYONE ACCEPTS that inflammation drives metabolic syndrome and obesity. And even among the idea’s proponents, no one claims that all inflammation emanates from the microbiota. Moreover, if you accept that inflammation contributes to obesity, then you’re obligated to consider all the many ways to become inflamed. The odd thing is, many of them are already implicated in obesity.

Particulate pollution from tailpipes and factories, linked to asthma, heart disease, and obesity, is known to be a cause of inflammation. So is chronic stress. And risk factors may interact with each other: In macaque troops, the high-ranking females, which experience less stress, can eat more junk food without developing metabolic syndrome than the more stressed, lower-ranking females. Epidemiologists have made similar observations in humans. Poorer people suffer the consequences of lousy dietary habits more than do those who are wealthier. The scientists who study this phenomenon call it “status syndrome.”

Exercise, meanwhile, is anti-inflammatory, which may explain why a brisk walk can immediately improve insulin sensitivity. Exercise may also fortify healthy brown fat, which burns off calories rather than storing them, like white fat does. This relationship may explain how physical activity really helps us lose weight. Yes, exercise burns calories, but the amount is often trivial. Just compensating for that bagel you ate for breakfast—roughly 290 calories—requires a 20-minute jog.

Then there’s the brain. Michael Schwartz, director of the Diabetes and Obesity Center of Excellence at the University of Washington in Seattle, has found that the appetite regulation center of the brain—the hypothalamus—is ofteninflamed and damaged in obese people. He can reproduce this damage by feeding mice a high-fat diet; chronic consumption of junk food, it seems, injures this region of the brain. Crucially, the brain inflammation precedes weight gain, suggesting that the injury might cause, or at least contribute to, obesity. In other words, by melting down our appetite control centers, junk food may accelerate its own consumption, sending us into a kind of vicious cycle where we consume more of the poison wreaking havoc on our physiology.

Of course there’s a genetic contribution to obesity. But even here, inflammation rears its head. Some studies suggest that gene variants that increase aspects of immune firepower are over-represented among obese individuals. In past environments, these genes probably helped us fight off infections. In the context of today’s diet, however, they may increase the risk of metabolic syndrome.

Biologically simple, processed foods may cultivate a toxic microbial community, not unlike the algal blooms that result in oceanic “dead zones.” In fact, scientists really do observe a dead zone of sorts when they peer into the obese microbiota. Microbes naturally form communities. In obese people, not only are anti-inflammatory microbes relatively scarce, diversity in general is depleted, and community structure degraded. Microbes that, in ecological parlance, we might call weedy species—the rats and cockroaches of your inner world—scurry around unimpeded. What’s the lesson? Junk food may produce a kind of microbial anarchy. Opportunists flourish as the greater structure collapses. Cooperative members get pushed aside. And you, who both contain and depend on the entire ecosystem, pay the price.

[This abridged version is provided for public use. See https://datadrivenviewpoints.com/fair-use-notice/]

Advertisements

How Wide is the Gender Gap – The Difference Between Mars and Venus

by Brian T. Lynch, MSW

 Are men and woman really so different?  Newly published research suggests that how men and women think may be even more different than we suspect!
Gender Differences
You have probably noticed that we humans come in two genetically distinct biological groups, males and females.  All other genetic distinctions are trivial by comparison.  We usually assume that our genetic differences are limited to these physiological distinctions. We take for granted that all social differentiation between men and woman is driven by these obvious biological traits.  More recently we have accepted that gender roles may be malleable characteristics molded in childhood according to the prevailing social norms.  Strip away the gender imprinting from society and we might find no psycho/social differences at all.
Support for this idea has come from scientific research which found that the frequencies with which various personality traits are exhibited in males and females are not so broad (see Hyde’s “gender similarities hypothesis”, 2005, Am Psychol 60: 581–592.).  This suggested a lot of overlap in the constellation of personality traits between men and woman.  At the same time there is a growing body of scientific evidence pointing to a genetic component in personality development.  This support the idea that both nature and nurture contribute to the person we become.
Now a new statistically sophisticated analysis of this earlier data on gender and personality traits appears to turned the previous findings upside down. In a paper entitled “The Distance Between Mars and Venus: Measuring global sex differences in personality,” three researchers named Marco Del Guidice, Tom Booth and Paul Irwing looked not at the frequency of distinct personality traits in males and females, but at multi-variant patterns of personality traits that appear to be associated with gender.  http://bit.ly/x2SsfL
In their analysis of these statistically correlated patterns, the researchers concluded there may be as little as a 10% overlap in the personality make-up of men and women.  This difference in gender personality traits is larger than previous differences found in other specific traits, such as aggression rates between the sexes, according to the researchers.  In their paper they also bring in the views of some evolutionary psychologist who hold that:

 divergent selection pressures on males and females are expected to produce consistent – and often substantial – psychological differences between the sexes.  By the logic of sexual selection theory and parental investment theory,  large sex differences are most likely to be found in traits and behaviors that ultimately relate to mating and parenting. More generally, sex differences are expected in those domains in which males and females have consistently faced different adaptive problems.” 

From their academic perspective the authors go on to say, Given the contrast between the predictions derived from evolutionary theory and those based on the gender similarities hypothesis, there is a pressing need for accurate empirical estimates of sex differences in personality.”  From an academic point of view this study will almost certainly intensify research and professional debate in this area of study.  Findings of this magnitude always do, and extraordinary claims require extraordinary proofs, which take time to develop.
From my perspective, if future evidence does convinces society that men and women have innately different templates from which our personalities emerge, this belief will have profound and far reaching consequences.  For now, however, this news simply makes for interesting parlor talk.

Lobbying Produced a 22,000% Return for Corporations per One Study

Is lobbying Congress a good investment?

This is normally a nearly impossible question to answer, but a unique set of circumstances allowed researchers to conclude that Corporate lobbying for a tax amnesty provision in the 2004 American Jobs Creation Act(AJCA) yielded a 22,000% return.  Yea, I would say it was worth it.

One reason why the question can’t normally be answered is that the financial information needed to answer the question can almost only be found on Corporate tax returns.  All tax returns are confidential and only the IRS can see them.  But a unique opportunity to study this question presented itself through a tax amnesty provision in the AJCA.

The University of Kansas School of Business ceased the opportunity.  Researchers found that they were able, in this unique situation, to publicly obtain all the information need to analyze the return on lobbying expenditures.  As stated in this study, “This is the first study to provide actual values of the financial savings arising from tax law changes, and the first to use data that has been audited by independent accounting firms.”

The study identified 496 firms that participated in the tax amnesty program and repatriation of foreign income.  They analyzed $298 billion of repatriations and the 93 firms that engaged in lobbying.  These 93 firms repatriated $208 billion (or 70% of the total). The lobbying group spent $282.7 million on lobbying expenditures and received $62.5 billion in tax savings, which represents a 220:1 return on investment. The study also summarizes the sausage making process as the AJCA bill made its way through Congress.

Cudos to the authors, Alexander, Mazza and Scholtz, and to the University of Kansas School of Business for this important piece of research.

Measuring Rates of Return for Lobbying Expenditures: An Empirical Analysis under the American Jobs Creation Act

 

Raquel Meyer Alexander

University of Kansas – School of Business

Stephen W. Mazza

University of Kansas – School of Law

Susan Scholz

University of Kansas – Accounting and Information Systems Area

April 8, 2009
Abstract: 
The lobbying industry has experienced exponential growth within the past decade. The general public, the media, and special interest groups perceive lobbying to be a powerful mechanism affecting public policy. However, academic research finds inconclusive results when quantifying the rate of return on political lobbying expenditures. In this paper we use audited corporate tax disclosures relating to a tax holiday on repatriated earnings created by the American Jobs Creation Act of 2004 to examine the return on lobbying. We find firms lobbying for this provision have a return in excess of $220 for every $1 spent on lobbying, or 22,000%. Repatriating firms are more profitable overall, but surprisingly, profitability is not a predictor of repatriation amount. Rather, industry and firm size are most predictive of repatriation. Cash on hand, a proxy for ability to repatriate, is not associated with the repatriation decision or the repatriation amount. This paper provides compelling evidence that lobbying expenditures have a positive and significant return on investment.

Number of Pages in PDF File: 36
Keywords: Multinational Firms, Corporate Taxation, Repatriation, Lobbying
JEL Classifications: F23, H20, H25, K34

Working Paper Series

GO TO THE WEBSITE AND DOWNLOAD THE FULL REPORT HERE http://bit.ly/Abj1Or


From the report:

“Dividing the estimated tax savings by the estimated amount spent on lobbying gives an estimate of each companies’ return on their lobbying investment. This measure gives an overall return of 220 times the investment. ((46,157.5 + 15,897.0)/282.7). That is, for every dollar spent on lobbying, there was a tax savings equal to about $220. In percentage terms, this is a 22,000% return.”
[Top 20] Companies Repatriating $500M or More
(105 companies total1)
Amount
Amount Repatriated/
Rank
Company
Repatriated
Total Assets2
Revenue2
1
PFIZER
37,000
30%
70%
2
MERCK & CO
15,900
37%
68%
3
HEWLETT PACKARD
14,500
19%
18%
4
JOHNSON & JOHNSON
10,800
20%
23%
5
IBM
9,500
9%
10%
6
SCHERING-PLOUGH
9,400
59%
114%
7
DU PONT
9,100
26%
33%
8
BRISTOL-MYERS SQUIBB
9,000
30%
46%
9
ELI LILLY & CO
8,000
32%
58%
10
PEPSICO
7,500
27%
26%
11
PROCTOR & GAMBLE
7,200
13%
14%
12
INTEL
6,200
13%
18%
13
COCA-COLA
6,100
19%
28%
14
ALTRIA GROUP
6,000
6%
9%
15
MOTOROLA
4,600
15%
15%
16
DELL
4,100
18%
8%
17
MORGAN STANLEY
4,000
1%
10%
18
CITIGROUP
3,200
0%
3%
19
ORACLE
3,100
15%
26%
19
WYETH
3,100
9%
18%

Micro Drones and the Future of Spying

Unlike the current unconstitutional practice of scooping up every phone call made in the US, at least a swarm of micro drones would need to have a specific target for their spying and reconnaissance work.  This story brings new meaning to the expression, “I’m being bugged!”

US military surveillance future: Drones now come in swarms?

Published: 20 June, 2012, 19:47
An image from NetworkWorld.com
An image from NetworkWorld.com

A small insect or a mosquito over your ear may now be much more than simply annoying. Those could easily be micro drones which now come in a swarm of bug-sized flying spies.

In an effort to create a hard-to-detect surveillance drone that will operate with little or no direct human supervision in out of the way and adverse environments, researchers are mimicking nature.

The University of Pennsylvania GRASP Lab showed off a network of 20 nano-quad rotors capable of agile flight, which could swarm and navigate in an environment with obstacles.

This is another step away from bulky heavily armed aerial vehicles or humanoid robots to a much smaller level of tiny remote-control devices. While current drones lack manoeuvrability, can’t hover and move fast enough, these new devices will be able to land precisely and fly off again at speed. One day the military hope they may prove a crucial tactical advantage in wars and could even save lives in disasters. They can also be helpful inside caves and barricaded rooms to send back real-time intelligence about the people and weapons inside.

A report in NetworkWorld online news suggests the research is based on the mechanics of insects, which potentially can be reverse-engineered to design midget machines to scout battlefields and search for victims trapped in rubble.

In an attempt to create such a device, scientists have turned to flying creatures long ago, examining their perfect conditions for flight, which have evolved over millions of years.

Zoologist Richard Bomphrey has told the British Daily Mail newspaper he has conducted research to generate new insight into how insect wings have evolved over the last 350 million years.

“By learning those lessons, our findings will make it possible to aerodynamically engineer a new breed of surveillance vehicles that, because they are as small as insects and also fly like them, completely blend into their surroundings,”the newspaper quotes him as saying.

The US Department of Defense has turned its attention to miniature drones, or micro air vehicles long ago.


Image from video of a swarm of Nano Qardrotors, posted at GRASP Laboratory website

As early as in 2007 the US government was accused of secretly developing robotic insect spies when anti-war protesters in the US saw some flying objects similar to dragonflies or little helicopters hovering above them. No government agency has admitted to developing insect-size spy drones though some official and private organizations have admitted that they were trying.

In 2008, the US Air Force showed off bug-sized spies as “tiny as bumblebees” that would not be detected when flying into buildings to “photograph, record, and even attack insurgents and terrorists.”

The same year US government’s military research agency (DARPA) conducted a symposium discussing ‘bugs, bots, borgs and bio-weapons.’

Around the same time the so-called Ornithopter flying machine based on Leonardo Da Vinci’s designs was unveiled and claimed they would be ready for roll out by 2015

Lockheed Martin’s Intelligent Robotics Laboratories unveiled “maple-seed-like” drones called Samarai that also mimic nature. US troops could throw them like a boomerang to see real-time images of what’s around the next corner.

The US is not alone in miniaturizing drones that imitate nature: France, the Netherlands and Israel are also developing similar devices.

An image from NetworkWorld.com
An image from NetworkWorld.com