Sunday Morning Live Appearance

The link is below. Jump forward 15 minutes if you want to see my little part.

http://www.bbc.co.uk/iplayer/episode/b00vr7lz/Sunday_Morning_Live_Episode_16/

The Captain's Agate Production

As many of you know, your Captain has many and varied hobbies and interests. He is the only ballroom dancing, salsa dancing, economist in the Twin Cities, but he is also a fossil hunter extraordinaire, a motorcyclist, an author (ahem), runner, gold-panner and all around cool guy. However, because I don't care to bore you, I have left my agate cutting and polishing out of the Capposphere on account I deem it one of the more nerdy hobbies I have. Only if I find an elusive and valuable "fairburn" agate do I mention it, otherwise (since agates are quite common) I leave my stone cutting and jewelry making out of the economics world.

However, the illustrious Natasha, after seeing a batch of agates I have made for a local jeweler DEMANDED I put these on the blog. I started to contest I shouldn't and on top of which I really didn't want to because I want to play Kane and Lynch 2, which then resulted in an argument that I knew I wasn't going to win and so I've decided to just put them here to make everybody happy (and to go the path of least resistance).



In the mean time click on Natasha to the right and donate some money to her heels and ammo fund.

Live on BBC1 This Morning

I’m going to be appearing on Sunday Morning Live - BBC1's topical ethical debate show presented by Susanna Reid, some time after 10.10am.

Response of plasma ASP to a prolonged fast

Response of plasma ASP to a prolonged fast - Abstract only unfortunately

OBJECTIVE: To determine the changes in the plasma level of acylation stimulating protein (ASP) during a one month total fast in female subjects with marked obesity.

DESIGN: Patients with marked obesity underwent a month total fast, before, during (2 weeks), and at the end of which, a variety of relevant metabolic parameters were measured.

SETTING: A metabolic unit of a teaching hospital.

SUBJECTS: 10 women with marked obesity were studied and the results compared with those in 16 age-matched controls.

MAIN OUTCOME MEASURES: Plasma ASP, lipoprotein lipids, apoB, free fatty acid, and ketone levels.

RESULTS: At baseline, fasting levels of ASP in the obese group were double that in control subjects (116 +/- 26 vs 53 +/- 30 nM P < 0.001). During the fast, ASP levels dropped progressively and were within the normal range at the end of the study (63 +/- 16 vs 53 +/- 30 nM pNS). In addition, there was a strong correlation between the plasma ASP at baseline before beginning the fast and the 4 week drop in ASP. That is, those subjects who had the highest starting ASP also had the largest 4 week drop in ASP (r2 = 0.644, P < 0.005). Of interest, as plasma ASP levels dropped, plasma free fatty acid and ketone levels rose and when all timepoints were considered, there was a significant inverse relation between plasma ASP and plasma free fatty acid (r2 = 0.295, P < 0.0002).

CONCLUSIONS: The pattern of responses during the fast is that of increasing mobilization of fatty acids from adipose tissue coincident with decreased activity of the pathway responsible for the storage of adipocyte triglyceride mass. The data are consistent, therefore, with the role proposed for ASP as a major determinant of the rate of triglyceride synthesis in human adipocytes and thus a potentially important factor in the pathophysiology of obesity.

It seems to me that it has been demonstrated in this, and other studies (that I've either shared or will as I get around to posting them) that ASP, as the highlighted conclusion above states, plays a major role in the Triglyceride/Fatty Acid cycle by controlling the the esterification (triglyceride synthesis from fatty acids + glycerol) rate.  This particular study demonstrates that ASP is not just involved transiently in the clearance of dietary fats (see, for example ASP action in vivo in humans), but rather has a basal/continual role in the on-going TAG/FA cycle.  Insulin primarily controls the release of fatty acids from the adipocyte, ASP seems to control the incorporation of fatty acids into triglycerides.  

On the GCBC Fact Check front:  Taubes ignored ASP and continues to ignore it.  It is worthwhile to note the date on this article:  1995.

Note that the obese women had higher fasting levels of ASP.  Fasting insulin tends to be elevated in the obese as well.  Taubes often repeats the carbs drive insulin drives fat storage.  That logic could similarly be applied to dietary fat, because as we know, fats (chylo) drive ASP drives fat storage.

Subdivisions of subcutaneous abdominal adipose tissue and insulin resistance

Subdivisions of subcutaneous abdominal adipose tissue and insulin resistance

This is a very interesting article.  They looked at not only visceral vs. subQ abdominal fat, but differentiated between two types of abdominal SCAT (subcutaneous adipose tissue):  superficial vs. deep.

There is a well described fascial plane within the SAT of the abdomen (18, 28), with the superficial adipose layer possessing compact fascial septa (Camper’s fascia), whereas the deeper layer of adipose tissue has more loosely organized fascial septa (Scarpa’s fascia).  Fat lobules of the two sites also differ. The superficial layer is characterized by small tightly packed lobules, whereas those of the deeper layer are larger and distributed in an irregular manner (28). The thickness of the deep layer appears more variable among individuals and especially in relation to obesity (3). The presence of these fascial planes and differences in histology are well recognized with respect to liposuction, which generally is targeted toward the deep layer (15, 23).  Given the anatomical basis for considering the two layers of SAT in the abdomen different and the ability to delineate the fascial plane utilizing CT (22), the current study was undertaken to examine these adipose tissue depots from a metabolic perspective. The related purpose was to address current controversies regarding the importance of subcutaneous abdominal adipose tissue in relation to IR.

I doubt the screen shot below will show up well, but thought to include them anyway:

Summary of Body Composition:

• Systemic FM (I'll use TotFM) was greater in the obese (obviously) and women compared to men in both groups.  
• Thigh FM (I'll use TFM) and superficial abdominal SAT (I'll use SASAT) was also greater in the women
• Deep abdominal SAT (I'll use DASAT) did not differ between genders
• Obese had 2-3X as much DASAT and visceral adipose tissue (VAT) vs. lean
• VAT was not significantly different between genders but trended towards greater VAT in males 
• DASAT was significantly greater crossectional area than VAT in the obese
• About 3/4's (mean ~76%) of the DASAT is located in the posterior (back), and this partitioning varied within a relatively small range (67-87%).  This distribution did not differ in obese v. lean or between genders.
• Anterior and Posterior SASAT is more evenly distributed around the circumference of the abdomen,  being ~55% front /45% back.
• The proportion of SASAT of all abdominal fat (I'll use TAFM)  was 45% v. 41% in lean women vs. obese women
• The proportion of SASAT of all abdominal fat was only 28% in both lean and obese men
• The proportion of DASAT of all abdominal fat did not differ significantly between genders but does appear to trend towards higher levels in men.
• The difference in proportion of DASAT (compared to TAFM) was statistically significant for obese v. lean in both genders:  32% LW, 37% OW, 36% LM, 44% OM
• VAT proportions were as follows:  23% LW, 36% OW, 20% LM, 27% OM.  This was stastically significant for obese v. lean but not for gender.
• VAT was highly correlated with DASAT (r = 0.76),VAT was more modestly correlated with SASAT (r = 0.43).   Statistical Aside:  When two variables are tested for correlation, the closer r is to 1, the tighter the correlation so this is a rather "huge" difference between the two types of SAT and their correlations to VAT.  

Summary of Relationships between Types of Abdominal Adipose Tissue Depots and Metabolic Variables:

• Glucose Rd (a measure of clearance rate) is negatively correlated with TotFM
• Glucose Rd was not significantly correlated with SASAT or TFM
• Glucose Rd was significantly negatively correlated with DASAT and VAT, the strength of this correlation (r) was similar between the two fat depots.
• Combined DASAT & VAT (considered together) were even more strongly correlated (r = 0.68) with decreased glucose Rd than either fat depot considered separately
• Both TotFM (this part is unclear, from the table I think it's TotFM, from the title of the section one might imply total truncal fat) and VAT accounted for 45% of the variance in insulin sensitivity.  Statistical aside:  This statement is related to the degree of correlation (r = correlation coefficient).  Let's use the common example of height and weight which are generally significantly correlated.  If you select an adult at random and measure their height, there will be considerable variability in the result.  If the r for the height weight correlation is 0.7 - made up number - then r^2 = 0.49 and we would say that 49% of the variability in weight is accounted for by its correlation to height. 
• DASAT is independently associated with insulin sensitivity (r^2 = 0.51) when TotFM (again not sure if this was total truncal fat), VAT & DASAT are included in the model.
• Controlling for either TotFM+VAT or TotFM+DASAT, SASAT was not associated with insulin sensitivity.
• The strengths of association for various fat depots and insulin sensitivity were similar to those of glucose clearance and rank:  VAT, DASAT > TotFM, total abdominal SAT > SASAT
• Correlations for glucose and insulin AUC (a measure of total exposure over a defined time period) were weaker.  But they were similar for VAT and DASAT and both greater than SASAT which seems to follow the correlation pattern of TFM
• This pattern was repeated for fasting insulin where VAT and DASAT (r = 0.57 and 0.58 respectively) were significantly greater than for SASAT and TotFM (r = 0.26 and 0.27 respectively)
• Other parameters are shown in the table below.  The pattern continues where SASAT "behaves" more similarly to TFM than do DASAT and VAT which behave similarly.

From the Discussion:

The current study was undertaken to examine the novel hypothesis that superficial and deep depots of subcutaneous abdominal adiposity, defined anatomically by a fascial plane that divides the two depots and differing in histological characteristics (22), might also differ in regard to their association with insulin resistance.  The findings clearly indicate that strong differences do exist. Superficial SAT manifests a powerful relation to plasma leptin but a weak association with insulin resistance, and in these and other respects, it follows a pattern observed for thigh subcutaneous adipose tissue, a depot generally regarded as a weak determinant of insulin resistance. In contrast, the deep subcutaneous adipose tissue of the abdomen manifests a robust relation to IR and other key aspects that define the insulin resistance syndrome (e.g., blood pressure, fasting insulin, and lipids); moreover, it does so in a pattern nearly identical to that observed for visceral adiposity. Therefore, from the perspective of understanding body composition and insulin resistance, these results indicate that it is not accurate to ‘‘lump’’ these two differing adipose tissue depots into a single category, but instead it may be useful to ‘‘split’’ the depots in accord with the anatomic demarcation of the fascial plane (18).

From a personal standpoint, I find this somewhat reassuring as I'm pretty sure that my "central adiposity" is of the superficial variety.  Therefore the shift from its former location (thighs/butt) to the belly may well not have any negative health implications as the behavior of this fat is metabolically similar to that of the depots from where it shifted.  

The Role Alcohol Plays in the American Conservative Movement

Understand that arguably the most important lesson you can learn in life is that it ends. And since it ends, why waste it worrying about things outside of your control.

Not to sound too macabre about the prospects of the country or the prospects of conservatism or the prospects of just plain and simple people who wish to excel instead of parasite during their finite lives, but basically, in the long term it doesn't look good. If you are a conservative you face a population that is increasingly spoiled, lazy, slothful, and worst of all, ignorant. They do not understand how the real world works, how the economy works and elect soothe sayers like the likes of Barack Obama or any other nickle and dime democrat that comes along and promises them puppies and money and flowers and the always available unicorn. Try as you might to convince them other wise and instill a milligram of sense or reality into them, they are too wedded to their "something for nothing" ideology and you are relegated to sit and watch the US collapse.

This is where the alcohol comes in.

Remember, the most important lesson you can learn in life is that it ends. This forces a choice upon you which I believe is the foundation to Dennis Prager's "Happiness Hour." You can either enjoy life or worry about it.

This is harder than it sounds, especially for conservatives. The reason why is that conservatives by and large care more about the country, their fellow man and society than their leftist counterparts do. Instead of just "saying" they want to do good things and do what's best for their children, and then go protest because they're bored and looking for something to do, they actually go the extra step and dedicate the through and "think-through-it-ness" that is required to determine whether certain policies will improve or worsen society. They don't just regurgitate bumper stickers such as "the rich get richer and the poor get poorer," they actually study economics and history to find out how to make everybody richer. The don't just go with their "feeling" or what they "think," they go out and actually find out the statistics, data and facts so that they KNOW.

With such a mentality, it's hard for conservatives to "let go" and just "enjoy the decline." I myself am guilty of this as I see this nation which once had a glorious past and now must watch it decline simply because its stewards (ie-the people) are spoiled, fat and lazy on our forefathers' success and therefore still write, blog, worry, fret about it today.

However, in the end I (as well as all of you) have to realize the reality of the situation. Too many stupid and ignorant people are in the country and have the right to vote. They don't care to look at the budget. They don't care to study history. They don't care to apply a level of intellectual honesty about them. They just want to say "warm fuzzies for everyone," "more money for schools/health care/the poor," "make the rich pay their fair share," not figure out how to pay for it, and then go back to watching "Glee" or "American Idol" while living off of borrowed money and producing nothing of real economic worth.

Now you can try to change this situation. YOu can try to point out the obvious. And you can try to point out the truth. But in the end you'll just be called a bigot, a racist, a neo-facist, or just a plain ole poopy head because NOBODY WANTS TO HEAR IT.

Ergo, what do you do with your finite life?

Well, starting up the next Standard Oil isn't an option.

Working hard and establishing a career isn't an option.

Working a normal amount and enjoying a normal family isn't even an option.

The only option left is to enjoy what remains of life. To feed off the remaining carcass of the now economically dead and defunct United States. To savor what meat has not spoiled and enjoy life to its fullest. And what better way to do that, while numbing the pain of watching the former greatest nation on the planet destroy itself than drinking?

That is why the Captain endorses the Drunken Conservatives.

The Drunken Conservatives are true economists at heart, because they know to maximize their utility and enjoy life.

They realize that they have an obligation to fight for what is right, to fight for the truth, and to fight for a future in which maybe the US isn't collapsing, but at the same time are not going to sacrifice what precious finite time they have on this planet worrying about something outside of their control. They are going to drink. They are going to enjoy life. They're going to kiss girls and they're not going to hyphenate their names. And there's nothing leftists or liberals can do to lessen that experience.

So visit the Drunken Conservatives.

Oh, and enjoy the decline!

Mandatory Reading for 14 Year Old Boys

It's lengthy, but certainly worth it. I don't necessarily agree with everything listed, but what I do agree with and why I posted it is because this is essentially the "Father Son Talk" that needs to happen today, but doesn't, simply because in the past there was no need for it.

Not to beget pity for the men of my age, but we were the first ones thrown into battle on this one and without a rifle and no intelligence. The above article would certainly arm the young men of today with some armament and therefore some hope of having a much more productive approach to courtship as they age.

Doctorate in English

Ah, majoring in a field where 99% of the population already has mastered the subject;

Facts of Capitalism!

What is amazing is that the first part of this series has 5,500 hits and this only has 1,100 hits.

PEOPLE WATCH THE WHOLE THING. The data is in the later parts like this one;

Widnes author Shaun Attwood to host launch party of new book at Eight Towers pub

Here's today's article in the Widnes Weekly News.

The Death of Men...Again

This is a long and lengthy analysis here written about another even longer article here. But in short it's one of the now common - "are men men anymore and are women beomcing the new men. And men are so stupid that they aren't earning degrees. How do we get men to work again? If only we knew?" etc. etc.

I will only add these two minor points that people keep failing to observe about this "death of man/mancession" phenomena;

1. PLEASE STOP WITH THE "WOMEN NOW EARN THE MAJORITY OF DEGREES" BS! They earn the majority of (sorry to say it, but it's true) worthless degrees. Yes, fine, wonderful. Masters in Communications. Masters in Social Work. Masters in Nose Picking. Yes, fine, you're all awarded degrees. Warm fuzzies for everyone! We're all winners!!!! Wow, can I get a degree in "Women's Studies?" Oh, no, wait, my brain would explode from the mundacity and idiocy of earning such a worthless degree because you're not learning anything nor will it serve you in searching for employment. Matter of fact all it will do is saddle some poor women with college debt with no increasing prospects for employment in the future.

Men still outrank women 4-1 in engineering and the sciences. Degrees that actually matter and have a practical application outside academia. Please stop with the "women out earning degrees" stuff unless you're going to talk about degree that translate into increased earnings and job prospects.

2. As the economy shifts from a private sector, capitalist based system to a public sector, socialist based system, of course women are going to become more prominent and higher earning than men. They major in the corresponding fields for government work. And given how the country keeps voting in more government spending and veritable socialists, it's going to continue to be a booming industry for women. Ironically, what's great about this is as the goverment grows and crowds out the private sector, it will be more common to see the "mechanic husband" with his highly paid wife who works at the social services department at the state making $80,000 and a pension that dwarfs his non-existent one. THat may sound "bad" for the once glorious male, but to quote Steve Martin from Dirty Rotten Scoundrels;

"I say it's time for a change. I say let them take care of us for a while!"

In the end, though ultimately, the economy will have to return to men or at least "manly" things because society cannot live off of an economy where everybody is a social worker or an elementary school teacher. People still want food, clothing, shelter, cars, Ipods, computers and electronics and protection. Gee, I wonder who specializes in the production of those things?

In the meantime, you know what to do;

Enjoy the decline, gentlemen. Enjoy that decline!

Changes in Energy Balance and Body Composition at Menopause

Changes in Energy Balance and Body Composition at Menopause: A Controlled Longitudinal Study  (Abstract only unfortunately)

This isn't LC related, but it is weight related.  And ... it's from the "It's Just Not Fair" department :-(

Abstract

Objective: To describe the effects of menopause on resting metabolic rate, body composition, fat distribution, physical activity during leisure time, and fasting insulin levels.

Design: A longitudinal comparison of metabolic changes in women who experienced menopause with changes in age-matched women who did not experience menopause.

Setting: General clinical research center.

Patients: An initial cohort of 35 sedentary healthy premenopausal women (age range, 44 to 48 years). After 6 years of follow-up, 18 women had spontaneously stopped menstruating for at least 12 months and 17 women remained premenopausal. No women received hormone replacement therapy.

Results: Women who experienced menopause lost more fat-free mass than women who remained premenopausal (−3.0 ± 1.1 kg and −0.5 ± 0.5 kg, respectively), had greater decreases in resting metabolic rate (−103 ± 55 kcal/d and −8 ± 17 kcal/d) and physical activity during leisure time (−127 ± 79 kcal/d and 64 ± 60 kcal/d), and had greater increases in fat mass (2.5 ± 2 kg and 1.0 ± 1.5 kg), fasting insulin levels (11 ± 9 pmol/L and −2 ± 5 pmol/L), and waist-to-hip ratios (0.04 ± 0.01 and 0.01 ± 0.01) (P ≤ 0.01 for all comparisons). Menopause did not affect energy intake, fasting glucose levels, or peak oxygen consumption.

Conclusions: Natural menopause is associated with reduced energy expenditure during rest and physical activity, an accelerated loss of fat-free mass, and increased central adiposity and fasting insulin levels. These changes may indicate a worsening cardiovascular and metabolic risk profile.          

If I'm reading this right, there is a combined change in energy expenditure of around 225 cal/day.
Yep ... no fair!!!

        

Hometown Launch Party and Live Television

I’m travelling up to Cheshire later today for the hometown launch party for Hard Time on Friday night. Over 200 people are expected. Further details are here. The Facebook page is here. Pics will be posted when they become available.

On Sunday morning, I’m going to be doing live television by way of an appearance on Sunday Morning Live - BBC1's topical ethical debate show presented by Susanna Reid and broadcast live between 10am and 11am every weekend. The prison debate will be the second debate on the show, which should take place between 10.20 and 10.40am.

Unacceptable Prison Sanitation at HMP Coldingley

I just did a radio interview for BBC Surrey on the subject of prisoners at HMP Coldingley having to defecate in plastic bags and throw urine and human waste out of their cell windows due to lack of access to toilets.

I stated that I had experienced similar conditions (see my first blog entry). I pointed out that when prisoners are treated like animals, some of them will behave like animals when they are released, and society will ultimately pay the price by way of more crimes and victims.

The inspectors at Coldingley classified the prison as safe - safe in the context of escape risk. If prisoners have to throw pots of urine and human waste out of the window, how safe is Coldingley in terms of disease risk, and how close are these prisoners to rioting in order to get the inhumane conditions improved? Unsanitary living conditions like these at HMP Coldingley enable diseases such as hepatitis, MRSA and staph infections to thrive in the prison system. The cost of treatment of diseases must be factored in when prisoners living areas are spattered with fecal matter and urine.

These conditions may satisfy the lock-them-up-and-throw-away-the-key brigade and allow the prison authorities to state that everything going on is "safe" to the public, but in the long run conditions like these cost more to society than any short-term savings.

When Liberals Try to Establish a Free Market

Wow, that's some kick ass liquidity there guys!

Just more proof it's never really been about "global warming" as much as it is a scam and a means to bring down the US. If people WERE serious about global warming then the above screenshot would be filled with historical data and price changes. Alas it is not and ergo economic proof global warming (at least the carbon credits aspect of it) was a scam.

hat tip

Can't Figure Out Why Newsweak is Losing Money

Cripes

Minneapolis, San Francisco, and Any Other Major Cities

I have said it before and I shall say it again;

Property taxes is the single largest unidentified threat to property prices and will undermine the housing and commercial property markets.

The reason is simple;

Cash flow appraisal techniques.

Understand what gives an asset (be it a house, a stock or whatever) value is the profits it generates. The cash flow it generates.

That's the ONLY reason any asset has value -because it can generate profits.

If your profits are slowly, but surely eroded away through taxation, you are eroding the one thing that gives the asset value. And ergo why, when the appraiser (or potential buyers) comes by to appraise your house, your rental property or your commercial property and sees property taxes lop off 60% AND INCREASING of your profits the remaining pittance of cash flow will not rationalize a highly valued price.

The ramifications go beyond the poor owner who gets less and less of the rental income.

Imagine what will happen to the bank's collateral.

Banks would be wise to start looking at the municipal government's budgets before accepting certain properties as collateral.

Enjoy the decline!

Absolutely Brilliant

HAR!!!

Good Thing Guns are Outlawed in Sweden

Otherwise they'd have shootings...oh, wait!

London Launch Event For Hard Time

A big thank you to everyone who attended the event last Thursday night at the Royal Festival Hall! Tickets sold out. We had a full house. Some people - including one of our most regular commenters here, Sue O - had flown in from America.

I ended up on the stage getting interviewed by Erwin James - a lifer who served 20 years. Erwin's rehabilitation through writing was so successful that he became a columnist for The Guardian while still incarcerated, and his prison memoir, A Life Inside, is highly acclaimed. His powerful presence did not go unnoticed. Many of my family and friends commented on what an excellent host of the talk he had been. Erwin picked up on everything going on in the audience, and adjusted the interview accordingly. He emphasized that the event was a celebration of prisoners redeeming themselves through art. Erwin also interviewed Matthew Meadows, whose excellent new book, Insider Art, showcases art by prisoners and is the first of its kind. The book is proving to be a powerful source of inspiration to all of the prisoners whose art it contains.

Sat on the front row, my parents were close enough to sabotage my feeble attempts at self-deprecatory humour.
For example, when I said, "I live the idle life of a writer. I get up whenever I want to," my mum interjected with, "He doesn't have a life. All he does is stay in his room and write."

The chief executive of the Koestler Trust, Tim, introduced and ended the talk. Koestler's Arts Mentoring For Released Prisoners program was his brainchild. That program transformed my life by way of my mentor Sally Hinchcliffe. Tim seemed moved to see the finished product (i.e. me) thriving thanks to Koestler's help.

Hammy and Wild Man (both in Hard Time) looked dapper in new suits (see photos in the blog below). After the talk, they disappeared into the dark and chilly London night like vampire bats, unable to fulfill all of the requests to autograph copies of Hard Time. Hopefully, they won't be so elusive at the hometown launch party for Hard Time this coming Friday. All are welcome. Details are:

Friday 29 October 8pm - 8 Towers Pub, Weates Close, Widnes, Cheshire, WA8 3RH Tel: 0151 424 8063

Hometown launch. Book signing, excerpts being read, and presentation with images. Special guests from Hard Time: Wild Man and Hammy.

Free event. No ticket or invitation required. Just show up on the night at any time.

Facebook page for hometown launch.

Over 200 people are expected, and the local radio station will be broadcasting live.

Pics From London Launch Event For Hard Time

The pics below:
1 Erwin James
2 Lynne, Garry, Aunty Lily
3 Hammy, Stephen Nash (formerly of Prisoners Abroad), Mum
4 Tim (Chief Executive of the Koestler Trust)
5 Inveterate commenter Sue O and family from Pennyslvania
6 Surrah, Gabriella and Hammy
7 Amy (from Phoenix), Yvonne and Peter (from Dublin)
8 Mum
9 Mike Hotwheelz (in Hard Time), Esther and Anna
10 Stephen Nash and Amy
11 Wild Man and Hammy (in Hard Time)
12 Charlie and Mum
13 The meal afterwards at Las Iguanas

Recession Medicine

A savvy Captain in his 20 something lieutenant youth would have plagiarized the lyrics from this song to make it look like he wrote a poem for a fair lass who was the object of his affection.




Now I just play video games.

Insulin Resistance ~ Taubes v. Frayn

Let's start with a discussion of :  Adipose tissue and the insulin resistance syndrome
(Another contribution from that "English Guy" ... Keith Frayn ...  note the date:  2001)

Obesity is associated with insulin resistance. Insulin resistance underlies a constellation of adverse metabolic and physiological changes (the insulin resistance syndrome) which is a strong risk factor for development of type 2 diabetes and CHD. The present article discusses how accumulation of triacylglycerol in adipocytes can lead to deterioration of the responsiveness of glucose metabolism in other tissues. Lipodystrophy, lack of adipose tissue, is also associated with insulin resistance. Any plausible explanation for the link between excess adipose tissue and insulin resistance needs to be able to account for this observation. Adipose tissue in obesity becomes refractory to suppression of fat mobilization by insulin, and also to the normal acute stimulatory effect of insulin on activation of lipoprotein lipase (involved in fat storage). The net effect is as though adipocytes are ‘full up’ and resisting further fat storage. Thus, in the postprandial period especially, there is an excess flux of circulating lipid metabolites that would normally have been ‘absorbed’ by adipose tissue. This situation leads to fat deposition in other tissues. Accumulation of triacylglycerol in skeletal muscles and in liver is associated with insulin resistance. In lipodystrophy there is insufficient adipose tissue to absorb the postprandial influx of fatty acids, so these fatty acids will again be directed to other tissues. This view of the link between adipose tissue and insulin resistance emphasises the important role of adipose tissue in ‘buffering’ the daily influx of dietary fat entering the circulation and preventing excessive exposure of other tissues to this influx

That abstract explains the somewhat paradox of the "metabolically obese thin people".   One function of adipose tissue is as a buffer of sorts to maintain appropriate circulating lipid levels.  This is important because of the basic physics of  immiscibility (non-mixing) of aqueous and non-polar liquids (think water and oil).   The over-stuffed adipocyte model makes sense even from a common sense POV.  If you think about a balloon being filled with air, it gets harder and harder the more full the balloon gets to blow more air into it.  Also, the mechanical integrity of the balloon deteriorates the more we stretch it.  When you look at an adipocyte, they sort of resemble balloons.  The "metabolic stuff" is located near the membrane on one side (other cells have nuclei central to the cell and mitochondria and other organelles throughout), sort of like the air inlet on a balloon.  One can expect the stuffed cell to have diminished integrity, etc.

Here is a rather simplistic model Frayn uses to describe the development of IR:

Note that Frayn implicates energy excess in the development of obesity.  From the discussion:

  

...If increasing fat storage in adipose tissue is associated with increasing insulin resistance, the simplest explanation might be something like that shown in Fig. 1; adipose tissue releases some signal (‘substance X’ in Fig. 1) that affects muscle and liver glucose metabolism (since these are the metabolic variables measured as insulin resistance)....

The most consistent evidence in favour of a candidate for substance X relates to fatty acids. (The general term fatty acids, rather than non-esterified fatty acids (NEFA), has been used for reasons expanded later.) ... NEFA release from adipose tissue is suppressed by insulin in both lean and obese individuals, but in obesity the process is ‘insulin resistant’ in that the dose–response curve is shifted to the right. NEFA release per unit fat mass is actually less in obese subjects than in lean subjects (effectively, it is down regulated by the fasting hyperinsulinaemia).  However, because of the increased fat mass, total NEFA delivery to the circulation is increased in obesity. Furthermore, if ‘lean body mass’ (including skeletal muscle and liver) is used as the denominator for NEFA turnover, then NEFA delivery to the consuming tissues is clearly increased in obesity. The ‘insulin resistance’ of adipose tissue lipolysis may be particularly relevant in relation to the delivery of NEFA in the postprandial period.  Despite high plasma insulin concentrations in response to a standard mixed meal, obese subjects fail to suppress NEFA release from adipose tissue at a time when it is completely suppressed in lean subjects.

So, in lean people, postprandial insulin *traps* fat in the cells, yet they are lean, so obviously this fails to result in net accumulation.  But in obese people, the insulin FAILS to trap the fat in the cells.  Thus there isn't this lack of available fatty acids to the hyperinsulinemic person as is sometimes portrayed by the authors of popular diet books.  

... in obesity the insulin-sensitive glucose-consuming tissues are subjected to an increased influx of fatty acids, and this increase is particularly marked in the postprandial period when adipose tissue, through ‘insulin resistance’, fails to protect other tissues from the influx of dietary fatty acids.

Frayn's description of insulin resistance is clearly of the "fat fails first" variety.  A theory consistent with the available evidence in 2001 (around the time of "Big Fat Lie", and LONG preceding the research and publication of GCBC).

So ... once again, I'm left to wonder how Taubes arrived at his version of the progression of insulin resistance in his GCBC book.  Starting on p. 394 of GCBC on Google books, (the entirety of the excerpts to follow are not available on Google, but I presume this page number corresponds to that of the hard copy).

"Over the years, prominent diabetologists and endocrinologists -- from Yalow and Berson in the 1960's through Dennis McGarry in the 1990's -- have speculated on this train of causation from hyperinsulinemia to Type 2 diabetes and obesity.  Anything that increases insulin, induces insulin resistance, and induces the pancreas to compensate by secreting still more insulin, will also lead to an excess accumulation of body fat.

That highlighted sentence is simply not true.   Neither carbohydrates nor proteins are associated with insulin resistance.  Indeed the only carb associated with IR is fructose, and fructose is also the one carb that doesn't elicit an insulin response.  

Taubes goes on to discuss James Neel "revisiting" his thrifty-gene hypothesis and how in 1982 Neel rejected it, instead suggesting three scenarios of physiological responses to excessive glucose pulses.   The first scenario involves a disproportionate quick insulin response.  The second involves the development of IR so that a proper insulin response fails to clear glucose from the blood.  But Taubes seems to focus on the third:

Neel's third scenario is slightly more complicated, but there's evidence to suggest that this one comes closest to reality.  Here an appropriate amount of insulin is secreted in response to the "excessive glucose pulses" of a modern meal, and the response of the muscle cells to the insulin is also appropriate.  The defect is in the relative sensitivity of muscle and fat cells to the insulin.  The muscle cells become insulin-resistant in response to the "repeated high levels of insulinemia that result from excessive ingestion of highly refined carbohydrates and/or over-alimentation," but the fat cells fail to compensate.  They remain stubbornly sensitive to insulin.  So, as Neel explained, the fat tissue accumulates more and more fat, but "mobilization of stored fat would be inhibited."  Now the accumulation of fat in the adipose tissue drives the vicious cycle.

Note:  Neel's exact words are presented in quotations, Taubes' words fill in.  Based on my fact-checking of some of Taubes' other references, I'm not at all sure Neel actually stated that fat becomes IR last.  But, presuming Taubes' characterization of Neel's work is accurate, this is clearly counter to Frayn's work above.  (See also The Progression of Insulin Resistance and Fat Fails First?)   However do note that even Neel's sequence of events begins with over-eating of carbs and/or in general.  This is counter to the whole "but why do we overeat" nonsense, and the whole "fat accumulation drives us to overeat, not the other way around".  IOW, Taubes inadvertently (as he does numerous times in GCBC) provides references/evidence counter to his unnecessary "alternate hypothesis",  and Critical Conclusion #5.

This scenario is the most difficult to sort out clinically, because when these investigators measure insulin resistance in humans they invariably do so on a whole-body level, whic is all the existing technology allows.  Any disparities between the responsiveness of fat and muscle tissue to insulin cannot be measured.

FALSE

• Subdivisions of subcutaneous abdominal adipose tissue and insulin resistance ~ 2000
• Tissue-specific insulin resistance in mice with mutations in the insulin receptor, IRS-1, and IRS-2 ~ 2000
• Plasma Fatty Acids, Adiposity, and Variance of Skeletal Muscle Insulin Resistance in Type 2 Diabetes Mellitus ~ 2001
• Insulin Resistance – What Is It and How Do We Measure It?
• Tissue-specific insulin resistance ~ 2004

I could list many MANY more.   Dated in the 90's and such.  This is a big problem with GCBC that I've had since I first heard someone extol it's virtue of highly referenced extensive research.  SOOOOOO much of that is 40+ years old, and Neel's work referenced here was over 25 years old at the time of GCBC's publication.  

Insulin Resistance – What Is It and How Do We Measure It?  This is an equine publication from 2009, but a review of older works.  

Clearly the understanding of IR and it's progression pre-dated GCBC.  If only Taubes had bothered to do such research?  Perhaps Taubes hadn't yet heard of or become acquainted with Keith Frayn?  Unfortunately he can't claim that b/c he cites Frayn in GCBC.  

I can only conclude that this is an example of the "scholarly incompetence" Taubes seemingly prefers to cop to.  Or could it be selling books?  LOL ... how dare I suggest that!

People Who Will Never Save a Miner

Cripes.

Nor will they ever contribute an ounce of genuine real production to society, because, it's all about the crusade people. It's all about the crusade.

Comparative Fatty Acid Toxicity on Macrophages

Comparative toxicity of fatty acids on a macrophage cell line (J774)

In the present study, the cytotoxicity of palmitic, stearic, oleic, linoleic, arachidonic, docosahexaenoic and eicosapentaenoic acids on a macrophage cell line (J774) was investigated. The induction of toxicity was investigated by changes in cell size, granularity, membrane integrity, DNA fragmentation and phosphatidylserine externalization by using flow cytometry. Fluorescence microscopy was used to determine the type of cell death (Acridine Orange/ethidium bromide assay). The possible mechanisms involved were examined by measuring mitochondrial depolarization, lipid accumulation and PPARγ (peroxisome-proliferator-activated receptor γ ) activation. The results demonstrate that fatty acids induce apoptosis and necrosis of J774 cells. At high concentrations, fatty acids cause macrophage death mainly by necrosis. The cytotoxicity of the fatty acids was not strictly related to the number of double bonds in the molecules: palmitic acid>docosahexaenoic acid>stearic acid=eicosapentaenoic acid=arachidonic acid>oleic acid>linoleic acid. The induction of cell death did not involve PPARγ activation. The mechanisms of fatty acids to induce cell death involved changes in mitochondrial transmembrane potential and intracellular neutral lipid accumulation. Fatty acids poorly incorporated into triacylglycerol had the highest toxicity.

 I could C&P the entire introduction to this paper but don't want to do that, so please go read it.  Summary:

• The FFA/NEFA are generally implicated in having toxic effects in non-adipose tissues, aka lipotoxicity
• Saturated fatty acids tend to be more lipotoxic
• Ectopic (non-adipose) triglyceride storage is somewhat protective but this remains under consideration as metabolites/intermediates of triglycerides (ceramides) are implicated in toxicity.
• Cell death contributes to the inflammatory properties of FA's
• PPAR-ɣ increases reduce inflammatory cytokines like IL's and TNF-α

Macrophage infiltration into adipose tissue in obesity is implicated in the inflammatory state associated with obesity.   It should be noted that this study was in vitro (e.g. culture dish) on a non-human (murine to be exact) derived cell line.   But the elevated NEFA associated with insulin resistance and T2 Diabetes would produce a "toxic" state within adipose tissue leading to macrophage death (and adipocyte death?). 

Cell death types:  

• Apoptosis, aka programmed cell death:  When functioning properly, this is the "natural" death of cells for cellular turnover in tissues, etc.  In cancer, apoptosis is short circuited leading to so-called immortal cells.  Some toxic conditions lead to disruption of the normal signals and pre-mature apoptosis.  
• Necrosis:  Premature cell death due to some - always detrimental - external source.  Necrosis initiates a greater immune response as dead cells must be engulfed and removed, and such cells rupture and "spill" more "stuff" into the surroundings than cells undergoing PCD.

Some exerpts:

In the present study, we evaluated whether the induction of cell death could be a mechanism by which FAs modulate macrophage function. Indeed, treatment with different concentrations of FAs was toxic to the macrophage cell line J774, as assessed by loss of membrane integrity and DNA fragmentation.  In most cases, the lowest concentration that caused loss of membrane integrity was the same that induced DNA fragmentation (Table 3), and the percentages were similar. These findings are indicative that necrosis and apoptosis occurred concomitantly.

... high FA concentrations cause macrophage death mainly by necrosis. This effect was also observed by others after treatment of different cell types, such as melanoma, leukaemia cell lines, lung carcinoma and fibroblasts, with high concentrations of FA [49–51].  The results of both loss of membrane integrity and/or DNA fragmentation shown in the present study suggest the following rank of toxicity on J774 cells: PA>DHA>SA=AA=EPA>OA>LA 

... The relationship between lipid accumulation and apoptosis has been demonstrated through a series of experiments with different cell lines [63–65]. Accumulation of excess FAs into the TAGpool has been postulated to divert these molecules from pathways that lead to toxic effects and, thus, lipid bodies may serve as buffers against lipotoxicity [19]. Treatment with all FAs led to an increase of lipid bodies inside J774 cells (Figure 2B).  Cells treated with non-toxic concentrations of the FAs exhibited higher granularity, indicating accumulation of lipid droplets that was observed by fluorescence microscopy. 

A look at Figure 1 indicates a threshold behavior for the toxic effects.

I have not addressed everything in this article and this post is sort-of half book marking, half just putting this out there as I had not seen a discussion of this nature before.

"I Read The Economist"

As older readers know I once religiously subscribed to and supported The Economist.

That is until they endorsed Barack Obama.

It was such an appalling display of a once great magazine aiming to boost their subscribership by sacrificing their standards so they could appeal to a fad and a brainwashed mass that I ended my then 11 year subscription to the magazine. It called into question the entire purpose and integrity of The Economist. Why would anybody, who was at least intellectually honest and cared about economic reality, subscribe to what had ultimately and quickly become tripe?

Well, if you look at an old post I had, it once again shows you the ole Captain might know what he's talking about.

The Economist is nothing but a biased, albeit, highly dressed up, left wing rag. Their readership is not about advancing economies and increasing standards of living and helping out humanity, it's about purchasing "The Economist" so they can say to their other UN diplomats and dignitaries that "they read "The Economist"" and sound intelligent. It's for liberal arts students to avoid real debate and say, "they read the economist" which then makes them the smartest person in the room. It's for middle aged people who decide to "upgrade" from the local paper and buck for a promotion when their manager realizes "Hey, he's reading THe Economist!"

Understand The Economist is NOT a legitimate publication. It is simply a "badge of honor" somebody can buy to make themselves sound intellectual. It's like buying a degree from a degree mill. You are better served reading various independent blogs and getting your economic data from economic databases than you are reading The Economist because "The Economist" (despite its name) isn't anything approaching what a real economist would do.

To remind you of this, I need not do anything else than post this chart;



Thus is the typical "Economist" subscriber and why you might as well not even bother ever subscribing to it. Because if you couldn't predict Obama would be bad for the US, then what kind of "economist" were you?

Answer - a shill

Recession Medicine

The Anti-Inflammatory Properties of Insulin

Some more articles presented without comment for book-marking purposes:

The anti-inflammatory and potential anti-atherogenic effect of insulin: a new paradigm

Intensive Insulin Therapy Exerts Antiinflammatory Effects in Critically Ill Patients and Counteracts the Adverse Effect of Low Mannose-Binding Lectin Levels

Anti-Inflammatory and Profibrinolytic Effect of Insulin in Acute ST-Segment–Elevation Myocardial Infarction

Shit Slingers V (The Early Years Part 6 by Polish Avenger)

Polish Avenger – A software-engineering undergraduate sentenced to 25 years because his friend was shot dead during a burglary they were committing. In Arizona, if a burglar gets killed, accomplices can get 25-year sentences.

Over the last entries we discussed Magnum and his willingness – nay, eagerness – to go places deep within the forbidden landscape of scatology and self-degradation. Yet even his fellow shit slingers were taken aback and slightly nauseated by his next innovation. In the fecal arms race, he crossed a line somewhere and became a poo kamikaze.

After the great splatterings that occurred as a result of his elaborate plumbing systems (see the last couple of posts), the guards caught on fairly quickly that even with the fellow naked and spread-eagled at the door, his was not a cell to be approached lightly! He would vary the pipe design and location, but ultimately one can only do so much to disguise several feet worth of device that’s equal parts Rube Goldberg and Dante’s Inferno (particularly one lower level featuring a river of boiling poo! Good old Dante…)

The guards began to very carefully inspect the cell front – from a distance, mind you – to ensure there would be no rain of liquid horror.
And they actually thought that would work.
Perhaps with a less determined, less deranged individual they may have reached an uneasy truce.
But this was Magnum. The sine qua non of shit slingers.

So one day after an inspection, they cuffed Magnum and escorted his naked ass to the shower. Once inside, it can be anywhere from 45 minutes to several hours before they come back to collect you. On this occasion though, it was about 45 minutes. Magnum cuffed up with no complaint, the shower door opened…and the guards were introduced to a whole new nightmare level of crazy.
I have to give the guy kudos. Most people in here try to make their time easier. Magnum went balls-out in the opposite direction and single-mindedly stuck to his guns that everyone was going to have a difficult time.

So, locked in a shower stall with nothing more than a little motel-style cake of soap, how would one befoul the guards?
Well, here’s one solution: Magnum proceeded to squeeze a hot log into his cupped hands and cram it into his mouth.
Yes, his mouth.
But wait, it gets better.
He then chewed, swirled, gargled and gnashed it around to get the proper runny consistency.
And then he sat down to wait.
I’m not sure how many of those 45 minutes he sat there, naked, alone, with a mouth full of his own pureed shit sauce.
But when the guards finally came to collect him and the shower door opened, he simply pursed his lips and became a human Dookie Uzi.
Damn!
Hygiene concerns aside, can you imagine his breath?

From all reports, this act so utterly shocked the guards that they just stood there in frozen amazement as poo-syrup slowly dripped down their face shields. Magnum sensed their momentary loss of composure and launched with savage glee into a flying tackle, trying to do some damage. He really didn’t as wrestling from the handcuffed and naked position is difficult at best. As usual, he was quickly maced, subdued, and led off to yet another holding cell. The real impact was psychological: what do you do with someone willing to go that far?
Wear lots of rubber clothing, apparently!

I got promoted (in name only) not long after, and so didn’t have to mop up Magnum’s holding cells any more. No, from now on I’d be mopping up his messes at the medical area and many other peoples’. And some of the staff members were quite nearly as bad as our Lord of the Shit Slingers.

Click here for Shit Slingers IV.

Our friends inside appreciate your comments.

Post comments and questions for Polish Avenger below or email them to writeinside@hotmail.com To post a comment if you do not have a Google/Blogger account, just select anonymous for your identity.

Shaun Attwood

Insulin: Endogenous Cardio-Protector?

Is insulin an endogenous cardioprotector?

Presented without comment, except to say that hyperinsulinemia is not the problem, it's what causes the hyperinsulinemia.  That being insulin resistance!

Visceral fat and insulin resistance – causative or correlative?

Having been introduced to "the English guy" aka Keith Frayn, I've discovered a rather extensive, as well as diverse, body of work by this researcher.   I'm sure to be sharing more in the coming weeks.  

Visceral fat and insulin resistance – causative or correlative?  (link is to full-text PDF)

The association between abdominal fat accumulation and risk of chronic diseases, including type II diabetes and coronary heart disease, has long been recognized. Insulin resistance may be a key factor in this link. Many studies have pointed to an association between insulin resistance and intra-abdominal fat accumulation (visceral obesity). However there is no clear proof of a causal link between visceral fat accumulation and insulin resistance. In assessing the probability of a causal link, it is useful to consider potential mechanisms. One such potential causal link is the release of non-esterified fatty acids from visceral fat into the portal vein, so that they have direct effects on hepatic metabolism. Visceral fat has been shown in many studies to exhibit a high rate of lipolysis compared with subcutaneous fat depots. However, if the idea that visceral fat releases fatty acids into the portal vein at a high rate is examined critically, a number of difficulties appear.  Not least of these is the fact that continued high rates of lipolysis should lead to the disappearance of the visceral fat depot, unless these high rates of fat mobilization are matched by high rates of fat deposition. There is far less evidence for high rates of fat deposition in visceral adipose tissue, and some contrary evidence. Evidence for high rates of visceral lipolysis in vivo from studies involving catheterization of the portal vein is not strong. If this potential link is discounted, then other reasons for the relationship between visceral fat and insulin resistance must be considered.  One is that there is no direct causal link, but both co-correlate with some other variable. A possibility is that this other variable is subcutaneous abdominal fat, which usually outweighs intra-abdominal fat several-fold. Subcutaneous fat probably plays the major role in determining systemic plasma non-esterified fatty acid concentrations, which are relevant in determining insulin resistance. In conclusion, there is at present no proof of a causal link between visceral fat accumulation and insulin resistance, or the associated metabolic syndrome. The possibility of co-correlation with some other factor, such as subcutaneous abdominal fat accumulation, must not be forgotten.

Hmmmm.... Co-correlation.  

This article discusses essentially 5 types of "central adiposity", so I might suggest an alternate title of "Central fat and insulin resistance".

• Intra-abdominal, aka Visceral Fat:  mesenteric and omental (pot-belly) in the front, and perirenal/retroperitoneal (as you see on my diagram these are different depots but described as the same in the article, so I take their intention to be non-subQ back fat).
• Subcutaneous:  anterior (paunch) and posterior (love handles)

Here is a good diagram of where each of the various adipose depots are located:

Some excerpts:

A number of studies have been aimed at identifying which of these various abdominal depots is most closely associated with insulin resistance. This is problematic since the subcutaneous and intra-abdominal depots are themselves correlated ...

One approach used specifically to examine the contribution of the intraabdominal depots has been to select subjects with large or small amounts of intra-abdominal fat, but to match them for total body fat and for subcutaneous abdominal fat.... this approach seemed to show that intraabdominal fat accumulation is associated with insulin resistance ... [but in this] study the groups did also differ in subcutaneous abdominal fat (by 11% on average) ...  the complementary experiment, matching for intra-abdominal fat and comparing people with high and low amounts of subcutaneous abdominal fat, has not been done. 

Another approach is to study a large number of people and use correlation analysis.  Studies using this technique show that the closest correlation with insulin resistance is seen with the subcutaneous abdominal depots.   Interestingly, these studies seem to show that the posterior subcutaneous depot is more closely associated with insulin resistance than is the anterior depot ... perirenal depot in these studies is clearly not associated with insulin resistance.

There is, then, a clear association between abdominal obesity and insulin resistance. Some studies suggest that the intra-abdominal or visceral depots show the closest link with insulin resistance, although others do not, and more evidence on this point is needed. However the observation of a link between abdominal obesity and insulin resistance does not mean that the former causes the latter. It could mean that insulin resistance causes abdominal obesity, or that both abdominal obesity and insulin resistance co-correlate with some other factor. 

Here's a summary of the results/conclusions for each of the five fat types:

1.  Anterior SubQ (aka paunch, muffin top, belly roll, over the belt flop):  Associated with IR

2.  Posterior SubQ (aka love handles, haunches):  Associated with IR, stronger than ASQ

3.  Omental (aka beer belly, pot belly) & 4.  Mesenteric:   Associated with IR but the Portal Theory (that these depots release NEFA into the portal vein therefore have a direct effect on the liver is not born out by in vivo studies.  "Some studies suggest that the intra-abdominal or visceral depots show the closest link with insulin resistance, although others do not"

5.  Perirenal:  Not associated with IR

Sat Fat --> PUFA = Less SubQ Belly Fat?

Mostly a bookmarking post, but I found this interesting

Substituting dietary saturated fat with polyunsaturated fat changes abdominal fat distribution and improves insulin sensitivity

For some reason I can't C&P the abstract.

They analyzed the results of 5 weeks on diets rich in sat fat vs. PUFA (described as spreads and oils, presumably high in omega 6 and probably some transfats :( ) on T2's, obese and non-obese subjects.  The study size was small, but I think most readers will be as surprised as I was by the results.

All of the PUFA groups had less subcutaneous belly fat at the end of the 5 weeks. This was statistically significant in the non-diabetics, both obese and non-obese.  Visceral fat either decreased or stayed the same. This was statistically significant for the diabetics, but not the non-diabetics.  

The PUFA group seemed to eat less, but total body weight didn't change.  Not sure what that's about.  Could be underreporting or a slower metabolism?  In any case, if this can reduce belly fat .....

Insulin sensitivity IMPROVED on the PUFA diet.  

This goes counter to that n=1 "study" by the journalist that altered her diet to consume O6's that has been making the LC rounds lately.  

Omega 3's

Effects of Omega-3 Fatty Acids on Lipids Glycemic Control in Type II Diabetes and the Metabolic Syndrome and on Inflammatory Bowel Disease, Rheumatoid Arthritis, Renal Disease, Systemic Lupus Erythematosus, and Osteoporosis           Summary

This is a summary of all the research this group could find about O3's.  Just putting this here to bookmark and FYI.

Left Wing Labor Economics

Because to them 0 jobs that pay $100,000 a year is better than 75 jobs that pay $25,000 per year.

Because There's No Faith in the Future

I love this chart.


You couldn't have a bigger stimulus than this to prompt investment and economic growth. Interest rates have never been lower (since the Fed started tracking 30 year mortgage rates) and housing prices are a mere fraction of what they were a year ago.

The problem is why isn't this translating into economic growth or at least a stabilizing factor in the housing market? I'll give you the answer;

There's no real hope.

You see, in order for a person to take on a large purchase such as a house and a large responsibility such as a 30 year mortgage, they have to have faith that their investment is going to pay off in the end. Not that the house is going to go up in value, but that it doesn't tank in value either. You throw in property taxes that continually go up, property maintenance, insurance, etc., you can see why people are a bit leery of buying a house. It's a liability, not an asset.

Go on the investment side and you see another angle. Banks won't even loan money out in the first place. Why? Because they're not certain about the economic future of the nation. Still stinging from the housing collapse (not to mention this newest "signing scandal"), they are reluctant to loan money out for housing. Anybody try to refinance their homes recently at these historically low interest rate? I'm sure some of you have only to be denied because you;

1. Were self-employed.
2. Had a decrease in your income
3. Wore blue socks on Tuesdays

Running scared from the housing crisis, banks are now perhaps OVERLY cautious and are just keeping their capital ratios close to their hearts.

Then there's the business side of things. Well if home buyers can't get financed, then certainly businesses and entrepreneurs will!

Heh, heh. Sadly they see no reason to invest because once again, there does not seem to be any genuine hope or faith in the future economy. They might go and invest in China. They might go and invest in Chile. They might go and invest in Brazil. But why invest in Japan-Circa-1990-Part II?

You see, you can have all the "stimulus" you want and pretty words from Barry and low interest rates, but without faith in the future of the economy, nobody is going to avail themselves of these opportunities because the prospects of an adequate ROI doesn't warrant it. Matter of fact, if the cost of debt capital is 3.5%, that implies investors and businesses don't even expect that paltry of an amount in today's economic climate.

At this point I would normally go on about how eliminating the corporate tax rate and making it constitutionally PERMANENT would flood the economy with real investment and hope for the future. But of course this is like shouting into the hurricane. My readers understand the reason for such a policy, but it is the masses of idiotic Americans who have been brainwashed to loathe those "evil" corporations.

And so I merely just point out the economic humor and irony of seeing interest rates so low, yet no growth and then laugh at the people who wonder why there isn't any economic growth, who in the same breathe blame the "corporations" for all their problems and want nothing more than to "make them pay their fair share" (all while wondering why their 401k isn't going up).

Enjoy the decline!

Just Another One (by Shane)

Shane - Denied psychiatric medication by ValueOptions, Shane turned to illegal drugs financed by burglaries. For stealing a few hundred dollars worth of goods, he was sentenced by Judge Ron Reinstein to eleven years. Shane is the author of the blog Persevering Prison Pages.

It was November 1999. The citizens of Phoenix were in a panic. Murders were on the rise, and the “Sonic’s Bandits” had a body count of at least 7.

The Sonic’s Bandits – two cousins armed with high-power semi-auto handguns – had been on a murderous rampage, robbing and shooting people at Sonic’s fast-food restaurants, an AutoZone, and various other businesses.
Seconds after the “hot-call” tone broadcast on the South Mountain Precinct police channel, the call went out: “Subject with a gun. Family barbeque restaurant, 23rd Street and Broadway. Suspect is a black male. Blue jeans. North Carolina hoody.”
An officer happened to be passing the restaurant: “Four-thirty-one-frank, I’m 23 on the location.” He parked next to the restaurant. Approaching the restaurant, the officer spotted the suspect standing at the counter looking up at the menu. Entering the building, the officer thought, Probably just another citizen calling 9-1-1 out of fear of the Sonic’s Bandits.

The suspect coolly glanced over at the uniformed officer. “What’s up,” he said, and went back to looking at the menu.
“What’s up,” the officer responded, approaching the man. “Can I talk to you for a second?”
The man put his hand in his right front pants’ pocket. “Sure, what’s up?”
“Sir, get your hand out of your pocket, put your hands on your head and interlace your fingers.”
The man complied.
“Sir, do you have any weapons, guns, knives or grenades on you?” The officer began to frisk the suspect.
Another officer entered the restaurant behind the man.
The first officer felt a pistol in the man’s pocket. “Gun!”
The man broke free, spun around and elbowed the officer in the face, breaking the officer’s nose. Reaching into his pocket, he tried to pull the gun. The second officer grabbed the man’s hand, trapping it inside the pocket. The first officer swung viciously, hitting the suspect in the face and head in order to disable the threat.
The suspect was unfazed by the blows, and continued to hit both cops repeatedly with powerful punches.
Breaking away from the fight, the first cop drew his sidearm from three feet away. “Nine-oh-one-george,” he yelled, expecting the second officer to recognize the radio code for a shooting and to stand clear. His training had kicked in and he wanted to neutralise the threat with a close proximity headshot.
But the second cop remained in the line of fire.
The first holstered his gun, and radioed, “Nine-oh-seven!” in a panic, the code for “Officer needs immediate assistance,” and jumped back into the fight.
After a knock-down drag-out three-minute fight, several other officers arrived and helped subdue the man.

After searching the man, and finding a second gun in his waistband, the first officer was putting him in his patrol car when the man told him something that he’ll never forget.
In a calm matter-of-fact tone that sent chills down the spine, the man said, “You should be pleased with yourself. You just got one of the Sonic’s Bandits.”
Still unsure, the officer said, “Yeah, right. What’s your problem?”
“Officer, when you walked in the door I was about to shoot you in the head. I’ve killed so many people. I’ve capped my family a few days ago even. You should be dead right now.” The man described how he had murdered his mother and brother.
The officer had been on the scene of those murders just days earlier. He now knew that the man was a Sonic’s Bandit, and that he had cheated death once again.

The officer in this true story is a friend of mine, who, years later, would sadly become addicted to prescription pills and get sent to prison for forgery and obtaining narcotics by fraud. His 11½ year career and military service in Iraq as an army medic with 2 Purple Hearts and a Bronze Star didn’t matter when he was sentenced to 2 years in prison. Drug addiction sees no race, sex, color, creed… or occupation.

Click here for Shane’s own blog

Click here for the first blog about Shane at Jon's Jail Journal

Some of Shane's prison stories:
What Comes Around
Convict Justice
Fighting For No Good Reason

Our friends inside appreciate your comments
Post comments for Shane below or email them to writeinside@hotmail.com To post a comment if you do not have a Google/Blogger account, just select anonymous for your identity

Shaun Attwood