The HR "Wish List" and Courting "Wish List" are Inexorably Intertwined

It is links between two seemingly unrelated things that start to show you the odd and sometimes amazing psychological, financial, sociological, economic, etc., relationships that exist in the world and helps bring about your understanding of the world to a clearer fruition.

One of which I hit on recently and went on at length about, but just found this whilst looking for means of employment which further proves my theory;



It's identical (not "similar," not "akin to,") but IDENTICAL to the girl/s who complain "there just aren't any good men."

Notice the year this was posted - Mid Year 2010.

REALLY????

1 in 5 jobs go unfilled because they CAN'T FIND A QUALIFIED EMPLOYEE?????

And nearly HALF of the organizations in your firm lack qualified workers????

ALL WITH UNEMPLOYMENT AT 9.6%, let alone UNDEREMPLOYMENT IN THE HIGH TEENS?

Really? there's NO QUALIFIED CANDIDATES AMONG THE MILLIONS OF UNEMPLOYED PEOPLE OUT THERE.

Mayhaps I suggest there is a little bit of impossibility in both HR's and women's "requirement list" for potential suitors, be it for a job or a romantic suitor? That asking for a man who is 6'2" or taller, makes lots of money, loves his mother, wants to go to church, but is a bad boy in bed, but not unless you say so, who likes to write you poetry, votes liberal, but is a man's man is about as probable as finding the candidate with 10+ years uninterrupted and progressive experience with a masters in blah blah blah blah (PhD preferred, of course) and billions of certifications who is going to work for an average wage and travel 90% of the time and have no social life out of work?

But, no, no. That CAN"T be it! You keep on going. You keep waiting for that perfect candidate to come along who magically has 8 years of experience in a software that has only been on the market for 3. I mean, there's no WAY charlatans and con artists would ever get through your impenetrable filtering and screening process and just tell you what you want to hear just so they can get the job. I mean it's just like dating, right? Nobody has EVER passed through that shield of yours that was unqualified, and CERTAINLY nobody who was ever qualified did you ever shoot down only to regret later.

Of course.

That never happens.

Heh heh.

Enjoy that decline, people. Enjoy that decline.

I Found This on the Floor of a Public School

Though I don't like to admit it (for it is charitable and therefore commie in nature), I do seminars at a local high school to teach juniors and seniors about various aspects of personal financial management. You know, simple things like 401k's, retirement, how you should pay for college, budgeting, etc., meaningful stuff that would actually help them in the real world unlike "Psychology" or "Peace Studies" or the bevy of "requisite" classes they force down these poor kids' throats to graduate.

Regardless, neither here nor there, it was a later seminar and by the time I packed up my LCD projector, I left the classroom and the school was deserted. I'm sure a janitor was on the grounds somewhere, but I could tell I was all of 3 people on the entire campus. And off in the corner of my vision I noticed a sole piece of paper laying on the ground that somehow didn't get swept up. So I walked over to where the paper was and picked it up.

It was a report of LBJ. I decided to keep it, bring it home, scan it in and then share it with you guys.


Now I used to substitute teach and I used to teach college econ, but I learned a long time ago, where the student has the ability and just chooses not to use it or if that student is a genuine idiot, it doesn't matter, you have to deal with the effective reality of their work.

Sadly, this is the generation I'm relying upon to produce the wealth to pay for my social security.

Cripes.

Horses Correlate with Bankruptcies

What do I keep telling you about horses?

I wonder if she tried to pledge them for collateral like one borrower I had the displeasure of underwriting for a while ago?

Understand people (but more importantly, BANKERS), if your client lists horses in the "assets" column of their balance sheet and NOT the liabilities section of the balance sheet, then you need to have those financial statements re-audited.

Reversing beta cell dysfunction

Mostly a bookmarking post, but indicates the possibility of "curing" type 2 diabetes.

Genipin inhibits UCP2-mediated proton leak and acutely reverses obesity- and high glucose-induced β cell dysfunction in isolated pancreatic islets

• 
  

  Summary

• Uncoupling protein 2 (UCP2) negatively regulates insulin secretion. UCP2 deficiency (by means of gene knockout) improves obesity- and high glucose-induced β cell dysfunction and consequently improves type 2 diabetes in mice. In the present study, we have discovered that the small molecule, genipin, rapidly inhibits UCP2-mediated proton leak. In isolated mitochondria, genipin inhibits UCP2-mediated proton leak. In pancreatic islet cells, genipin increases mitochondrial membrane potential, increases ATP levels, closes K_ATP channels, and stimulates insulin secretion. These actions of genipin occur in a UCP2-dependent manner. Importantly, acute addition of genipin to isolated islets reverses high glucose- and obesity-induced β cell dysfunction. Thus, genipin and/or chemically modified variants of genipin are useful research tools for studying biological processes thought to be controlled by UCP2. In addition, these agents represent lead compounds that comprise a starting point for the development of therapies aimed at treating β cell dysfunction.

On a related note, claims have been made by Dr. Eades and others, that on low carb diets a metabolic advantage is achieved at least in part by wasting fat calories because high fat diets increase uncoupling proteins in mitochondria.   If true, and this impacts UCP2 in beta cells, this would not be a good thing!  If I'm reading this summary correctly, excessive UCP2 "short circuits" the beta cells and keeps them from releasing insulin.  

Capitalism Is NOT Why the US Will Fail

Cappy Cap readers should be really appreciative of me. Not because of the awesome economic commentary I make. Not because of the super awesome economic foresight I have. But rather because I screen out the most inane and idiotic comments that would shorten your life expectancy with high blood pressure if you did indeed read them.

Of all of them, however, there is one no more blood boiling than this one;

"CAPITALISM is what is going to destroy the US."

or

"The US will fail because of capitalism."

This is, without a doubt, the most ignorant, intellectually dishonest and patently wrong comment I receive.

Now, I'd like to go into detail in my typical arrogant prose, but since this post is very important, I am instead going to be brief and succinct in the hopes of keeping most people's attention. It really is just too important not to read. The reason why is that when the US economy DOES ultimately collapse, I want it recorded here exactly what kind of economic system was in place before knee-jerk college students just regurgitate what their aging hippie professors tell them.

First, we are no longer a "capitalist" economy. We are a mixed or socialist economy (please don't make posts on technicalities and nuances in the terms - they will be ignored). We have the same public sector spending as Norway (the left's favorite nation - and probably more thanks to BO).


Second, we have the world's second highest corporate tax rates at roughly 40%. An effective rate of 32.5% (I'll give a shinny nickel to a liberal who can explain the difference between the two, instead of just relying on this fact as a talking point when talking about corporate taxes).


You throw in dividend taxes and you're roughly at a 50% overall tax rate.

Third, understand the US economy and people's standards of living were growing fastest when tax rates (as measured by government spending as a percent of GDP) were the lowest. Standards of living have gone down as the US economy has become socialist;


(*I get a lot of confusion on this chart. The rolling 20 year includes 20 years worth of data. The data point I place in the middle, which is why it seems there is 10 years of data missing on the start and end of the blue line)

Fourth, understand the majority of government spending is NOT for governance, but rather income transfers, which is the epitome and definition of socialism.



Fifth, understand that it is these income transfers and entitlements into the future that are the primary reasons for our current and future projected deficits and is the primary reason we are facing bankruptcy as a nation. These are DISTINCTLY socialist policies. NOT CAPITALIST.




Now there are more statistics, but the above is enough. I cannot make it any clearer and I don't have to because it's not a matter of opinion. It's a fact. It is SOCIALISM that is destroying the United States. NOT capitalism.

Therefore, please, I beg of you idiots who just regurgitate the above inane comment, since you have the right to vote, stop being ignorant and start getting educated on economics. This isn't a "choice." This isn't a "fun little game we're playing." And this isn't some "crusade" where you try to impress the hippie grunge chick at the coffee bar by extolling socialist tripe as you try to pass it on as "virtues." You future is at stake. Your current state of unemployment is a direct result of your own ignorance. And if you'd want any kind of future for your children, let alone yourselves, knock it off with the childish "ranting" and "protesting" and grow up. The country depends on it.

Owning Property in Major US Cities Is a Liability

I've said it before, and you people didn't listen to me, but owning property in major US cities is a liability. Not only because of perpetually dropping housing prices, but the risk just isn't worth it. You have to deal with leftist regulations, the threat you'll be forced to abide by progressively increasing municipal environmental regulations (recycling, insulation, heating requirements, etc), and as capital and labor flights out of the city to the burbs, you will face a Detroit like environment. But the biggest risk, property taxes.

You don't think AFSCME and SEIU at the local government shops are going to take pay cuts do you?

And you don't think good liberals in major cities are going to vote in any kind of republicans or politicians that will cut spending, do you?

Ergo you can expect your property taxes to go up regardless of the economy and the value of your property, which will directly force your property value down further because the net cash flow it could feasible generate has gone down.

Smart people will make moves like this.

Daddy, Where Do Jobs Come From?

A repost of a classic in that unemployment is still around 10% and I'm guessing some of you might like jobs about now.

Jobs, it seems is becoming a very important issue as we seemed to have shed 5 million of them recently and are on the precipice of the worst recession since 1929. But fear not, for our president elect has a plan and it’s quite simple;

“More jobs.”

Yes, that’s about it, we’ll just “create” more jobs.

Now 3^rd grade logic would tell you something is wrong. You can’t put your finger on it. Maybe you can’t full explain it. But you have this twingling sensation in the back of your head that you know something just ain’t right. That it ain’t as simple as;

“Just creating more jobs.”

It’s the same kind of twingling sensation you got back in school when you said, “Well why don’t we just print off more money.”

You intuitively knew something had to be wrong with that solution, but you perhaps couldn’t explain why. And thus it’s the same thing with Barack’s plan to create new jobs.

His idea for this massive infrastructure (and Keynesian) investment gives us all the same twingling sensation in the back of our heads. Why, if it was that simple, to just build roads, bridges and splurge more on education, what were we getting all worried about in the first place? Why are the stock markets so low? Why don’t we create jobs right now today? And so, since we all intuitively know it can’t be that simple, let me explain why. Let me explain to you where jobs come from.

Jobs come from one thing; demand.

Demand for goods and services currently existing or yet to exist. For example I demand food, a good that already exists. I also demand a hovercar and a clone of Jennifer Anitson, a good and service that have yet to exist. Regardless, if the product or service exists or can be created, and there is demand for it, then there is the potential for jobs to be created.

But demand must be met with supply and here is where the actual jobs are created. In order to supply these goods and services an entrepreneur or a company must hire people to help provide those goods and services. This includes everybody from the head of the company managing the firm to the suppliers, vendors, laborers, admins, marketers, accountants and anybody else required to bring these services to reality. However, there is a key element to make this all happen and that is profit.

Oh yes, that “evil” profit.

For you see, no entrepreneur, nor company, nor corporation is even going to bother going through the trouble of setting up the venture in the first place unless they are actually paid for it. And before you start berating these “evil capitalists” to have the temerity to demand recompense so that they may earn a living, you might want to look at yourselves in the mirror because no laborer (let alone you) is going to work unless they are compensated too. So just accept the fact we’re all financial whores, not out of evil or greed, but because it’s necessary for us to live and survive.

Regardless, immediately we see a problem with, not so much Obama’s infrastructure plan, but his fiscal policy in that he is going to raise taxes on not only the rich who employ the majority of people, but also corporations. Envy them and hate them all you want, increasing taxes on them will lower the incentive for them to invest, let alone start a new venture in the first place. And with the rapidly integrating global economy, if they really do have a great idea, why would they set up shop here in the first place? Ireland has a 12.5% corporate tax rate. Dubai has 0%. Russia has a flat tax. And “communist” China has a 20% corporate tax rate.
The good ol’ US o’ A has a 39% corporate tax.

So even though we haven’t addressed Obama’s specific infrastructure jobs creation plan, it’s quite possible other parts of his fiscal policy will impair it or destroy more jobs than it creates, simply because it destroys the incentive to create jobs in the first place; profit.

As for the specific plan itself, it’s not an issue of whether it will create jobs as much as it is a question at what cost.

Understand that to finance this infrastructure plan Obama has two choices; taxation or borrowing. And both options are going to cost jobs as well as efficiency.

In taxing people (no matter how “rich” they are) that takes money that would have been invested or spent anyway which would have created jobs as well. So if you tax the “rich jewelry dealer” an extra $50,000 so 2 employees in Obama’s Civilian Conservation Corps can pour concrete for a bridge, that’s all fine and dandy except for the fact the jewelry dealer now had to lay off his assistant and his admin to compensate for the cut. Congratulations, you created a big fat zero net new jobs.

Borrowing is no better in that the money borrowed by the government to finance the infrastructure jobs creation plan could have been borrowed by a company, an entrepreneur or even an individual to be used to create a new company, expand a factory or just plain spent, all of which would have created jobs too. Congratulations. You not only borrowed money and destroyed as many jobs as you created, but you’ve managed to increase interest rates as well! Thanks!

But the real cost is this, and is often the forgotten about or never-thought about aspect of economics, and that is efficiency. Specifically, as it relates to production.

If the money was left in the hands of the people, the people could then spend or invest that money as they saw fit and to their best benefit. Allowing people to make their own decisions as to how to expend their resources is the best way to make sure the goods and services produced in the economy are those that most benefit the people and increase standards of living the most. Of course, people make mistakes. The sickening, gluttonous binge of using one’s home equity as an ATM machine which has brought upon this financial crisis in the first place is a perfect example where the people will make mistakes. However, for all their flaws, recessions and depressions, free markets, ie- the people have historically been proven to be the best determinants of what to be produced.

Governments have not. And herein lies the flaw in Obama’s advisor’s plan; taking massive amounts of resources either through taxation or borrowing, takes money out of the hands of individuals and puts it in the hands of government. People now no longer get to decide what to spend their now dwindling resources on, and are instead forced to spend it on roads, infrastructure, and schools they may not need.

Now people may rightfully point out that things like roads, bridges, infrastructure, etc., are hardly foolish investments, and they’re right. But again the question is at what cost? Who would be better judges of how to spend this money and who would do more to help the economy out of recession;

A handful of bureaucrats and former Fannie Mae and Freddie Mac advisors now consulting a no-real-world-experience-president-elect determining what the best use of your money is?

Or

300 million Americans who are intricately familiar with their own personal financial situation and the problems/opportunities they face?

This is where the real costs come in that what determines our standards of living is whether we use our resources efficiently to produce the goods and services we NEED. We just promised $700 billion (more like $2 trillion) to bailout those same Harvard ef-ups who ran Wall Street and the government into the ground. Could the people not have used a $700 billion tax cut? Would that not have solved our little economic growth problem? No, we’re stupid, we don’t know what we’re talking about, now shut up and give us the money.

Obama’s infrastructure plan is no different (although, I will admit spending the money on bridges and roads is infinitely wiser than bailing out Ivy League deadbeats). We don’t know what’s best for us. You don’t need that money. Give it to us and we’ll build shinny new roads and bridges. Just what you wanted. No, not that new icky gross Pontiac Solstice that would ACTUALLY HELP OUT DETROIT WITHOUT A TAXPAYER BAILOUT. No Captain, that’s not what you want. You want an addition to the elementary school named after Barack Obama where a newly hired teacher will brainwash…errr….I mean “educate” the children about the evils of capitalism…errr…I mean “global warming.” That’s what you want.

It is this that is the true cost to this Keynesian nightmare. The loss of productivity and efficiency causing American’s standards of living to go down. Not because of a loss of jobs (for I’m optimistically assuming this infrastructure plan will ONLY destroy one job for each one it “creates”) but because the stuff we’re producing with it is not what the American people optimally want.

And finally, permit me a third point.

I know building bridges, though not optimal, is not a waste of money.

I know roads, albeit not optimal, are not a waste of money.

But notice how education was thrown in there?

Please. Please, just stop with the “we don’t spend enough on education.”

It’s a sickening lie and you’re not fooling anyone. By every measure, every stretch of the imagination we spend WAY TOO MUCH on education and the fact education is part of Obama’s jobs creation plan shows me just how inefficient this plan will be. Bridges, fine. Roads, fine. But more money for education would be on par with bailing out the losers of Wall Street and sub prime deadbeats.

Alas, appetizing as new roads and bridges are, it was the inclusion of education, above all else, that made me supremely confident the stork will not be bringing any new jobs to Obama with his little infrastructure plan.

Lipogenesis v. Adipose Mass Gain ~ Fructose

A while back I posted a summary of lipid vocabulary:  Lip-ocabulary.  I had hoped to address this sooner than now.

Another topic on my (rather long) list of how Taubes either misunderstands or misrepresents lipid metabolism and storage involves his use of terms related to "lipogenesis"  (e.g. fructose is the most lipogenic of carbs) to imply that it leads to fat accumulation.  

In his defense, there are any number of scholarly articles and texts that use the term lipogenesis to describe the "genesis" of fat stores.  However they do so in the context of discussions of adipose tissue and do not conflate de novo lipogenesis and fat storage.  Adipogenesis may not be exactly appropriate either, as this term is most correctly attributed to the formation of new fat cells.  But at least the "adipo" implies fat tissue, thus it might loosely apply to the genesis of adipose tissue (whether by proliferation or filling of existing cells) rather than the synthesis of lipids per se.

Where obesity is concerned, we're interested in what causes changes in adipose tissue mass: increases or decreases.

In the past few years, fructose has become the new "saturated fat", to where fructophobes will avoid even carrots!  This is due in large part to Lustig's alarmism, but Taubes weaves this into his lectures as well.   We are to equate fructose with alcohol because it is processed in the liver and consider it particularly fattening because fructose elicits the highest rate of DNL of any carbohydrate.  But just as carbohydrate per se is not uniquely fattening, neither is fructose per se.  It is the processed tasty vehicles either in liquid form and/or packing a caloric whollop that are.  Can you say ice cream?!

But back to the vocabulary, I've posted before demonstrating that lipogenesis does not contribute much to adipogenesis.  See:  Nutrient Fates after Absorption and Excess carbs converted to fat?   But lipogenesis -- the synthesis of larger lipid molecules from smaller molecules -- is not only an energy consuming process, it may also be thermogenic as I posted about here:  Fat Futile Cycling from Carb Excess (or more lay-friendly).

Bottom line, it is misleading to equate lipogenesis with fat accumulation in adipose tissue.

Hard Time Reviews by Prisoners No. 5: Long Island

Long Island - Promising young cellmate I taught to trade the financial markets. Released on the 11th of December '05 and rearrested February ’08. Alleged to have committed forgery and hit an officer with a car. He’s writing from Sheriff Joe Arpaio’s Lower Buckeye jail.

I received Hard Time yesterday and have finished it this afternoon. I read straight through almost all night. Bravo, my friend, well done! It was fantastic and the ending was heart wrenchingly beautiful. Your depictions of Towers jail and the Madison Street jail are superb.

Ironically sad, nothing has changed. The people you described are still here, but the names are changed.

Your description of your relationship with your fiancée, Claudia, has left me shaken and your mother’s trauma and her statement at sentencing brought tears to my eyes.

Reading your words to myself, my mind was hearing your voice. It was as if you were in the cell reading the book aloud to me. You have once again inspired me to reach within myself and pull out the best parts.

One of the things that impressed me the most was that the book wasn’t just about the jails that we live in, but the jails that the people who love us live in while we’re incarcerated. Claudia’s pain was so vivid, and you parents’ was unbearable.

The photos of you in the book look great. Freedom is definitely agreeing with you. Your devotion to Wild Man speaks volumes of your character. The photo of you two together looks great.

I’m letting my attorney read it next, then his legal secretary.

Good show, old boy!

Click here for the previous review in this series.

Click here for Long Island's previous blog.

Hard Time at Amazon UK. Hard Time at the Book Depository.

Raving Rabbids Movie

Will somebody over at Ubisoft please make a movie of the Raving Rabbids? Or at least a Saturday morning cartoon.

Anne Mini

There couldn't be a better introduction to the US version of Hard Time than the one written by Anne Mini. I am extremely delighted and fortunate that Anne - whose advice and blog has helped shape my literary development over the years - has taken the time to make such a wonderful contribution. Today, she has announced her contribution and posted some kind words about Hard Time to her blog here. http://www.annemini.com/?p=13486

US Hard Time Cover Revised

Knuckle Check (by Lifer Renee)

Renee – Only a teenager, she received a 60-year sentence from a judge in Pima County. Fourteen years into her sentence, Renee is writing from Perryville prison in Goodyear, Arizona, providing a rare and unique insight into a women's prison.

I was waiting for an officer to do the head count. Shadows kept passing by my door, which was not normal. I went to the door, and peered out of my window. On the lower run were dark droplets that I knew were blood. Instead of hiding my contraband, I checked to see what the guards were doing. They were making women step out of their cells one at a time. They were doing knuckle checks – and more. They were examining forearms and faces, and making the women pull their shirts up to reveal their stomachs and lower backs.

By the time they reached my cell, shirts were no longer being pulled up, which was good because I was ready to protest. It is most uncomfortable to be stared at by guards who look as if they are counting every pore on your skin.

They arrived at my cell. “Let’s see your hands!”
I held my hands out, palms down.
They checked for marks that would indicate I’d been fighting. Seeing none, they moved on.
After they had checked my neighbors, I jumped upon the toilet and called my neighbor through the 4”x4” vent above the toilet that connects the cells.
“Neighbor, Hope.”
She jumped onto her toilet. “Hi, neighbour.”
“Do you know what happened?”
“No, nothing,” she said. “Just a knuckle check.”

Usually fights in here do not happen quietly. I don’t know why, but women have a tendency to yell, scream, and make quite the scene. My door had been open, yet I didn’t hear a thing. I also didn’t understand why the blood wasn’t cleaned up if they didn’t want to go unnoticed.

Click here for Renee’s previous blog

Post comments for Renee 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

Happy Thanksgiving

Enjoy this thankful day with your familyand/or friends!   Eat, drink and be merry!!

How to Choose a Major

There's the hard way doing all your research, talking to people, listening to your idiotic guidance counselors that just want to blow smoke up your chute, etc.

Or just buying this book for $5 and reading it.

Paperback version if you don't have a Kindle here.

Exercise & Insulin Sensitivity I ~ IR in older populations

Just wanted to share two studies I came across relating exercise and cardiac fitness to insulin sensitivity.  I'm sure to add more to this series as I come across them.

I only have access to the abstracts for these studies.  If any of you have access to the full text, please consider sharing it with me via my email address in my profile.  Thanks!

Study 1:

Association of cardiorespiratory fitness with insulin sensitivity in overweight and obese postmenopausal women: a Montreal Ottawa New Emerging Team study

The purpose of this study was to examine the relation between insulin sensitivity and cardiorespiratory fitness in overweight and obese postmenopausal women. The study population consisted of 127 overweight and obese postmenopausal women (age, 57.7 ± 4.8 years; body mass index, 32.7 ± 4.7 kg/m2).

Subjects were classified by dividing the entire cohort into tertiles (T) based on insulin sensitivity expressed per kilograms of lean body mass (LBM) (T1, <10.9; T2, 10.9-12.9, T3, >12.9 mg/min per kilogram of LBM, respectively). Outcome measures were body composition (dual-energy x-ray absorptiometry), visceral adipose tissue (computed tomography), insulin sensitivity (hyperinsulinemic-euglycemic clamp), cardiorespiratory fitness (indirect calorimetry), lower-body muscle strength (1 maximal repetition), physical activity energy expenditure (doubly labeled water), fasting lipids, and inflammatory profile.

We found a significant positive relationship between insulin sensitivity and cardiorespiratory fitness (r = 0.25, P = .005). Moreover, cardiorespiratory fitness was higher in the T3 group compared to the T1 group (36.2 ± 6.1 vs 33.1 ± 5.0 mL/kg LBM per minute, respectively; P = .028). However, the difference was no longer significant after controlling for visceral adipose tissue or muscle strength.

Finally, cardiorespiratory fitness was an independent predictor of insulin sensitivity. High levels of cardiorespiratory fitness are associated with higher levels of insulin sensitivity in overweight and obese postmenopausal women. Moreover, visceral adipose tissue accumulation or muscle strength may be potential mediators of this relationship.

I'm presuming the more cardiorespiratory fit women got that way through some form of exercise, likely "cardio".  

Study 2:  Exercise-Induced Changes in Insulin Action and Glycogen Metabolism in Elderly Adults

Purpose: Although data suggest that physical activity is associated with decreased insulin resistance, recommendations for exercise training are not specific for age or level of obesity. Therefore, we examined the influence of moderate-intensity (50% of V̇O_2max) exercise training (MI) versus high-intensity (75% of V̇O_2max) exercise training (HI) on insulin-stimulated glucose disposal (ISGD) in elderly individuals.

Methods: Following medical examinations, 21 overweight (body mass index = 29 ± 1 kg·m^-2) elderly (74 ± 1 yr) subjects were randomized to 1) HI, 2) MI, or a 3) nonexercising control group. Subjects enrolled in HI or MI completed a 12-wk exercise training regimen designed to expend 1000 kcal·wk^-1. ISGD was assessed using a hyperinsulinemic, euglycemic clamp pre- and postintervention. ISGD was corrected for hepatic glucose production (glucose R_a) using a constant rate infusion of [6,6-²H₂]glucose and determined during the last 30 min of the clamp by subtracting glucose R_a from the exogenous glucose infusion rate. Nonoxidative glucose disposal was calculated using indirect calorimetry. Body composition testing was completed using dual energy x-ray absorptiometry.

Results: ISGD increased by approximately 20% with HI (Δ of 1.4 ± 0.5 mg·kg^-1FFM·min^-1). However, ISGD did not change (Δ of -0.4 ± 0.1 mg·kg^-1 FFM·min^-1) with MI and was not different (Δ of -0.2 ± 0.1 mg·kg^-1 FFM·min^-1) in the control group. Nonoxidative glucose disposal increased with HI (Δ of 1.4 ± 0.5 mg·kg^-1 FFM·min^-1), but there was no change in nonoxidative glucose disposal with MI or in the control group. No change in body weight or percentage of body fat was observed in any group.

Conclusion: In weight-stable subjects, MI resulted in no change in ISGD, and the improvement in ISGD with HI was completely reliant on improvements in nonoxidative glucose disposal.

This study looked at the influence of exercise on insulin resistance in weight-stable subjects - e.g. changes in IR cannot be attributed to weight loss.  It was the high intensity exercise that improved insulin sensitivity by increasing insulin stimulated glucose disposal, while medium intensity did not.  This is interesting because the activities were "standardized" to equivalent caloric expenditure of 1000 cal/week.  Since they were weight stable over 12 weeks, it is not mentioned in the abstract, but presumably intake was adjusted to compensate. Unfortunately, the abstract contains no details on the duration of exercise, although there's no mention that the HI was also interval training (HIIT).

Insulin resistance is associated with aging and menopause.  These two studies indicate exercise as a good strategy to maintain insulin sensitivity.

My First In-Store Book Signing - Waterstone's Warrington

I just got back from Cheshire, and all was not grim up north. I did my first book signing in a book store on Friday at Waterstones in Warrington. Many people were buying the book as a Xmas present for young people as a cautionary tale about getting involved in drugs and crime. Much to the amazement of the staff, they quickly sold out of books, and my mum had to bring more to the store. They're recommending me to the other Waterstone's, and I already got booked by the Manchester Deansgate one (Saturday March 19th), which is the biggest in the northwest. Hard Time is still riding high on Amazon, in part thanks to a mention in this months FHM.

Click here for the news story about my signing: http://www.warringtonguardian.co.uk/news/8682460.Former_prisoner_tackles_book_signing/

Aaron Clarey's New Baby Boy

Recession Medicine

I know the recession is "over," because, well the NBER said it was. All you losers who don't have jobs, shut up and quite whining. Just kidding. That's the Barack Obama/Nancy Pelosi in me talking.

For the rest of us real economists who know the recession isn't over, permit me another showing of Bing Crosby and Blue Eyes;

Because 0 Jobs that Pay $75,000 a Year is Better Than 75 Jobs that Pay $25,000 Per Year

So a court decided that the employees of a Wal-Mart in a town in Canada had the right to unionize.

Apparently, the union isn't too bright because the last time this happened, Wal-Mart closed the store down.

Ergo, what is the economic lesson to take away from this, ladies and gentlemen?

The wonderful logic of unions that zero jobs paying an imaginary $75,000 is better than 20 jobs actually paying $25,000.

Oats ... More Reader Input Requested

I'm being a bit lazy here because we're hosting Thanksgiving and stupid me decided to tackle some "spring like" cleaning and re-organizing.  So I thought I would ask for your help in answering the following question because my reading around the net has been conflicting.  Do oats contain gluten per se, or is it that most oats are contaminated by gluten from other grains processed by the same machinery or in the same facility (dust?).  

Thanks in advance!

Public Speaking Videos

In the two videos below, I'm at Regents College, London talking to a group of psychotherapists. It was part of a masterclass put on by Andrew T. Austin. Double click on the videos to get the full screen version.

 

Physiological, Pharmacological, and Nutritional Regulation of Circulating Adiponectin Concentrations in Humans

Physiological, Pharmacological, and Nutritional Regulation of Circulating Adiponectin Concentrations in Humans

Get this one while its free folks (until the end of the month)!  Adiponectin is an all-too-often overlooked hormone in the obesity and metabolic syndrome game.  

I haven't had time to read it thoroughly but it contains a wealth of information.  The graphic below summarizes the 17 page paper content:

Hmmmm... cheers everyone!  (booze is adiponectin friendly :) )

Legumes ~ Reader Input Request

I'm trying to reconcile the plethora information I keep coming across regarding the benefits of the Mediterranean Diet and similar with the shunning of legumes in the Paleo community (including peanuts and cashews).  There is a lot of info on toxic compounds in legumes.

I would be interested in any and all input on this topic, links I should check out, etc.  

Lately I've been upping my carb consumption slightly and have always enjoyed such foods as chili with various kidney beans, garbanzo beans (mostly in salads), and Mexican bean dishes.  I've already incorporated some of these into my diet (infrequently) to no ill effect, probably causing many of you to cringe and worry over my imminent demise.  ;-) ... or maybe not {VBG}.

Insulin Is an Anti-inflammatory and Anti-atherosclerotic Hormone

Insulin Is an Anti-inflammatory and Anti-atherosclerotic Hormone  (full text free until end of the month)

Fasting hyperinsulinemia is associated with an increased risk of atherosclerotic complications of heart attack and stroke. This has resulted in the concept that insulin may promote atherosclerosis in spite of the absence of any evidence that insulin is atherogenic either in the human or in experimental models. Recent evidence shows that insulin exerts vasodilatory, anti-platelet and anti-inflammatory effects at the cellular level in vitro and in the human in vivo. Since atherosclerosis is a chronic inflammatory process of the arterial wall, insulin may be potentially anti-atherosclerotic in the long term. More recent data on experimental atherosclerosis in the mouse shows that (1) insulin administration reduces the number and the size of atherosclerotic lesions in apo E null mice and (2) in IRS-2 null mice, the interruption in insulin signal transduction results in enhanced atherogenicity. Finally, the use of a low dose of insulin infusion in patients with acute myocardial infarction has been shown to markedly improve clinical outcomes, both in diabetic and nondiabetic patients. Our own most recent data show that a low dose infusion of insulin in patients with acute myocardial infarction induces a reduction in nflammation (C-reactive protein and serum amyloid A) and oxidative stress, and promotes fibrinolysis. We conclude that insulin is anti-inflammatory and potentially antiatherogenic and may be of use in the treatment of cardiovascular inflammatory conditions.

It seems that the demonization of insulin has followed much the same path as the correlation = causality logic of LDL and atherosclerosis.  Elevated LDL correlates with CVD, but there is not a whole lot of actual evidence demonstrating that the LDL itself directly causing atherosclerosis.   LDL remains a fairly reliable marker for determining risk (though it must be considered along with other factors), and whatever the flaws (and there are many) in cholesterol theories, this shouldn't be ignored out of hand.  If A causes B, and A causes C, then someone with B likely has C.

So with the insulin, we have hyperinsulinemia correlating with CVD, but as stated in the abstract above, there's little evidence that it causes it directly.  The "A" in this scenario seems to be elevated free fatty acids (NEFA/FFA) leading to "B" = hyperinsulinemia and "C" = atherosclerosis.  But in this case the correlation/causation connection may be even more convoluted.  Because there's an intermediate factor in all this -- the ever-increasingly apparent root of all evil: insulin resistance.  The way I see it is this:  Fat stores exceeding an individual's storage capacity lead to IR of the fat cells and/or excessive release of NEFA.  Elevated NEFA induces IR in peripheral tissues.  It is cellular resistance to insulin's inhibitory roles  in these cells that ultimately lead to metabolic dysfunction and/or cell damage/death.  In this regard, the relationship is not so much one of insulin not being the cause of atherosclerosis, etc., but the resistance masks the fact that it would appear that insulin is actually protective against it!  

Inflammation, shmimflamation!  :

Atherosclerosis is an inflammatory process.7 All the major classical risk factors for atherosclerosis, hypercholesterolemia, diabetes, hypertension, smoking, and menopause are associated with (and probably cause) inflammation. If high insulin levels are atherogenic, one would expect it also to exert part of its negative effect on the vessel wall through inflammatory processes. Recent evidence which we shall now review shows that just the opposite is the case, i.e., that insulin is anti-inflammatory.

The article goes on to summarize such research.  I'll let the more science minded read that for themselves (heck, I'm just too lazy at the moment to do a decent summary), but this section concludes with:

In view of the anti-inflammatory and vasodilatory effect of insulin, insulin resistance may be expected to be pro-inflammatory and a proconstrictor state. This indeed is the case.  Obesity,31 type 2 diabetes,32 and other insulin resistant states, such as polycystic ovary syndrome (PCOS),33 are pro-inflammatory and are associated with abnormal vascular reactivity and platelet hyperaggregability.  (clumping & clotting)

........... Insulin sensitizers have been shown to exert anti-inflammatory43–46 and anti-atherosclerotic effects.47,48  Thiazolidinediones (TZD) exert anti-inflammatory effects at the molecular and cellular levels. 

The article goes on to conclude as follows:

These facts, should encourage us to increase our understanding of these novel effects of insulin so that

(1) we have an improved conceptualization of inflammation in states of insulin resistance and the relationship of these states to atherogenesis;

(2) we explore the potential therapeutic role of insulin in inflammatory conditions, such as acute myocardial infarction; and

(3) we investigate novel potential therapeutic application of insulin sensitizers such as thiazolidinediones as anti-inflammatory agents.

I broke these out in more bullet form to address them.

(1)  I take this to mean the lipid hypothesizers need to rethink as much as the carbohydrate hypothesizers do. Both need to re-think the role of dietary composition (and total intake) in terms of its impact on insulin SENSITIVITY, not insulin per se.

(2)  Insulin is, as Martha Stewart would say, a GOOD thing.  There's much promise in using it.  Insulin therapies have evolved from slow acting secretagogues (substances that enhance insulin secretion), to pumps delivering a more consistent, physiological basal level in T1's etc.

(3)  OK, I'm probably in agreement with many who disdain the whole "this gives us more reason to look into more drugs" angle, but we have to be pragmatic about it.  A Type 1 does not make insulin.  In that regard, whatever technology allows them to mimic insulin levels in a normal person, I would be grateful for it.  Type 2 is a far more varied diagnosis as the degree of irreversible damage (as opposed to suppressed function) cannot be assessed with mere fasting glucose levels or tolerance tests.   If you're hyperinsulinemic, you still have functional beta cells.  Temporarily giving them a rest with LC while you lose weight and reverse the IR that is causing the elevated insulin is a great strategy.  But if you cannot adhere to this, or if LC doesn't result in the desired weight loss, then it may well be worthwhile to at least temporarily look into pharmaceutical intervention that allows for insulin to "do its thing".  I wonder, even, if insulin might be helpful to the hyperinsulinemic T2 -- enough exogenous insulin may keep the pancreas from having to work overtime to produce the elevated levels that your body is telling it to anyway.  There's nothing about the hormone that is deleterious!!!!!!!!

Book Signing Friday Nov 19th

I'll be signing books at Waterstones in Warrington from 11am until 3pm. Anyone in the northwest who wants to attend is welcome. Here's the full address:

23-24, Golden Square Shopping Centre
Warrington WA1 1QE
0843 290 8675

7 Famous Inmates Who Completed a Degree from Prison

7 Famous Inmates Who Completed a Degree from Prison

An Evening Meal (by the Occult Killer)

Dubbed the Occult Killer by the media, Brandon is serving 6 to 12 years in the Commonwealth of Pennsylvania Department of Corrections. His crime: he killed his best friend in a drunk-driving accident. When police investigators discovered Gothic paraphernalia in his bedroom, they naturally concluded Brandon had committed a sacrificial murder for the benefit of Satan.

The kitchen is on this string of heinousness, so I’ve been hanging back and eating 7-11 cuisine. Tonight was sausage simulate with cheese-flavored snack product on Keefe cracker-flavored flatbreads, expertly sliced with my ID card. Whatever that processed garbage is made out of, it’s pretty good. On top of that I have some freeze-dried milk and Imperial Ice Cream Credits. A few nights ago I had some raspberry cheesecake ice cream. Slammin’. I swear, we eat whatever beefs it on the highway. Say if a poultry truck overturns that day, chicken dinner for a week. Same thing when the crows start to disappear. Very odd…

Click here for Brandon's previous blog.

Click here for Brandon's review of Hard Time.

Caffeine and Insulin Sensitivity

Caffeine and Insulin Sensitivity  (full text PDF free till end of the month)

A number of reports have observed that acute caffeine ingestion decreases glucose tolerance and insulin sensitivity, and have raised the question whether its increased consumption throughout the world in the form of coffee and cola beverages might be of public health concern in the development of type 2 diabetes. Although some epidemiologic studies have found strong associations between coffee intake and detrimental lifestyle factors that favor obesity and diabetes, it is interesting that in spite of this, they have demonstrated that increased coffee consumption is associated with a decreased risk of developing type 2 diabetes.  When lifestyle confounders are taken into account, individuals consuming 6 cups coffee per day have at least 50% less risk of developing type 2 diabetes than those consuming 2 cups per day. Although it is perhaps premature to recommend increased coffee or caffeine intake to prevent the development of type 2 diabetes, there is little or no evidence to warrant the recommendation that it should not be a part of a normal healthy diet.

This is an interesting summary article.  In the section entitled Caffeine and Carbohydrate Metabolism, a case for acute caffeine consumption impairing glucose tolerance by inducing insulin resistance (decreases glucose uptake) is laid out which goes counter to the results of the coffee study highlighted above.   Perhaps it's something else in the coffee?  

More modest inverse associations were also observed for decaffeinated coffee consumption, caffeine intake from noncoffee sources, and total caffeine intake, as well as the incidence of type 2 diabetes, suggesting that caffeine and other components of coffee contribute to this inverse relationship.

Seems in part the case.  The authors discuss the conflicting short term "laboratory measured" effects and those seen in epidemiologic studies.

... it is very obvious that the results and conclusions of the acute and epidemiologic studies do not agree, and this illustrates the problem of extrapolating shortterm observations to a chronic disease (with an etiology that is influenced by a variety of interacting genetic and lifestyle factors.)

This seems even more surprising given the rather strong correlation between coffee intake and other lifestyle factors that are deleterious such as drinking, poor diet, etc.  Below I've summarized in bullet point fashion how the authors believe increased coffee intake decreases the risk of developing T2:

• Caffeine stimulates resting metabolic rate.  It could be as simple as fewer coffee drinkers getting overweight?
• Caffeine increases epinepherine
• Caffeine + epinepherine act together to promote lypolysis leading to an increase in plasma free fatty acid levels. (<- at first glance this might seem to not be a good thing)
• C+E have a thermogenic effect.  (thus the FFA's are likely readily oxidized with the boosted metabolism)
• The combined effects increase lipid turnover (less ROS hanging around??) "which may in the long-term have beneficial effects on body weight, body composition, and substrate use that could help to prevent the development of glucose intolerance, insulin resistance, and diabetes."

They go on:

However, such arguments are very speculative, and it may well be that the observed acute effects of coffee or caffeine on glucose tolerance and insulin sensitivity are suppressed by habituation to its repeated consumption.  Indeed, repeated caffeine consumption over 5 days induces complete tolerance to its effects on blood pressure, heart rate, and, in particular, blood glucose concentrations.52 

They also consider the other components of coffee:

• Coffee contains many bioactive compounds, most of which have as yet unknown metabolic effects.
• Coffee contains a quinide that improves insulin-mediated glucose uptake in rats
• Phenolic compounds in coffee influence GIP (glucose-dependent insulinotropic polypeptide) and GLP-1 (glucagon-like peptide I) levels.  (These two peptides are called incretins and are associated with beta cell proliferation and decreased apoptosis (death) 

"Consequently, the combined physiologic effects of coffee’s many components may well be very different from that of one of the components studied alone."

Posted by CarbSane after her third very large mug of coffee 8*)

Does Metabolic Syndrome hamper weight loss efforts?

This study would indicate that, if anything, it helps (??Say what!!??)


Does the Presence of Metabolic Syndome Influence Weight Loss in Obese and Overweight Women? (PDF full text free until end of the month)

Background: It is known that weight loss is benefi cial for obese and overweight subjects with metabolic syndrome. Very few data exist, however, about whether the presence of metabolic syndrome and insulin resistance (IR) infl uence the response of these subjects to weight-reducing interventions. The current study intends to examine whether the presence of metabolic syndrome and its components could infl uence weight loss in obese and overweight women during a short-term, dietary-based intervention program.

Methods: A total of 107 women aged 49.1 ± 13.5 years old, with a body mass index (BMI) greater than 25 were studied. The subjects were prescribed a low-fat diet plus weight-reducing drugs when necessary.

Results: After 3 months, the subjects with metabolic syndrome lost more weight than those without (6.62% vs. 4.50%; P < 0.05). There was a positive correlation between the percentage of weight loss and the number of the components of metabolic syndrome present at baseline (Spearman ρ = 0.329; P < 0.01). Furthermore, patients in the quartile with the highest homeostasis model assessment index (HOMA-index) lost more weight than the remaining subjects (8.17% ± 3.34 vs. 5.59% ± 3.87; P < 0.05). These results were signifi cant, even after adjustment for the medical treatment prescribed.

Conclusions: Obese and overweight patients with metabolic syndrome showed a greater reduction of their body weight, compared to the patients without metabolic syndrome. The components of the metabolic syndrome present at baseline correlated positively with the percentage of the weight loss. Finally, the patients with the highest levels of HOMA-index at baseline lost significantly more weight than those with lower levels of this parameter.

I find this somewhat surprising.  It would seemingly go counter to what one expects given the effectiveness of low carb diets and how an even higher fat lower carb/protein version (e.g. fat fast, Silver Cloud Diet) is usually advocated for the more hyperinsulinemic.  This study looked at a low fat diet.  One would also think that if insulin resistance (which is the underlying factor in metabolic syndrome) causes obesity then the obese/overweight with IR should have greater difficulty losing weight.  

Things that make you go hmmmmmm.

Aspirin for Insulin Resistance? Part II: Not so fast

A follow-up post to a post a while back:  Aspirin for Insulin Resistance?

I just came across the following article that has me thinking "not so fast":   The effect of salicylates on insulin sensitivity

Although the carefully performed study by Kim et al. provides new insight into the mechanisms of fat-induced insulin resistance, we would like to caution against the preliminary conclusion concerning beneficial effects of salicylates on insulin resistance. First of all, in contrast to the findings of Kim et al. in the triglyceride (TG) infusion model in the rat, earlier studies in human volunteers using hyperglycemic clamp techniques reported increased insulin resistance by salicylate compounds (3,4). These findings suggest that the effects of salicylates may depend on the experimental model, and possibly on the species studied.....

The schematic below summarizes the various actions and possible impact on insulin sensitivity for salicylates, the text under this is the legend from the schematic.

The effects of salicylates on insulin resistance. There is significant overlap between the intracellular events induced by TGs (or FFAs) and TNF regarding the mechanisms of insulin resistance. Both stimuli activate IKK-β and decrease insulin-induced tyrosine phosphorylation of IRS-1; both increase intracellular ceramide concentrations, which leads to inhibition of Akt/protein kinase B activation and inhibition of GLUT-4 translocation. These effects induce a state of insulin resistance. The effects of salicylate compounds on these pathways may be divergent. That is, they may improve insulin resistance by blocking the activation of IKK-β (top), or they may worsen insulin resistance by inhibiting PG synthesis and thus potentiating TNF release (bottom). In addition, inhibition of PG will decrease synthesis of leptin, which is known to improve insulin sensitivity by stimulating IRS-1–associated PI 3-kinase activity. The beneficial effect of leptin on insulin action is thus decreased (bottom)

In conclusion, the influence of salicylate compounds on insulin sensitivity is multifactorial and involves both beneficial and deleterious effects. This should not preclude patients from taking low-dose aspirin to prevent cardiovascular disease (15), but more basal and clinical studies are needed before recommending higher dosages of salicylates for the treatment of type 2 diabetes itself.

Oh well.  Does make you kinda wonder what other meds might do.

Swinging Bachelor Economists Don't Buy Gold

I had a buddy ask me about "red neck gold" - ie - investment alternatives to gold because, well, frankly people can't afford $1,400 an ounce. I presumed he had gotten the term from the internet, but when I went on the internets I could not find the term nor any article about it. It actually surprised me because I would have thought "red neck gold" was a logical next step in the evolution of investing given our chaotic economic times and the prohibitively expensive prices of gold. But then again things that seem "logical" to me are horribly super-advanced complex things doctorates in econometrics need super computers to model and figure out, so permit me once again to lay down some serious old school, blue collar economic genius.

First you must ask yourself why does gold have value or become a refuge during dire economic times. The answer? Simple - it's money. Not in the "fiat" paper dollar bill, sort of money. It IS money. And what I mean by that is it has the qualities and traits that make it a good money;

1. It has an intrinsic value. Most men scoff at gold as merely a mineral that looks shiny and pretty. Well who likes shiny, pretty things? Women! Who likes women? Men! And so history is filled with instances where men slay other men for gold because of..ahem... let's just say "biology."

2. Gold is divisible. You can divide it, mint it, press it. Cars aren't. You can't just come into Whole Foods with a Prius and get a bag of groceries and use a car as payment. It would not be fair to you. You need something that can be a smallish or smaller unit of measurement (ergo a dollar, a shilling, a yen).

3. Gold sticks around for a while. It doesn't degrade or mold or deteriorate. Is it any surprise metals were the original money? Copper, gold, silver, nickle. You can put a bar of gold in the ground and because it's half life is something like 40 billion years, you're still going to have 99.9999999999% of it 10 years later.

4. It's universally accepted. You of the highest alpha-male bachelor order may have no practical use for gold (technically, nobody does), but you're no schmoe to turn down a free bar of gold. It's worth something to somebody. So you may not use it, but you could use it to buy yourself something that is valuable like an X-Box 360 or a trip to Vegas or the Captain's super awesome book on the housing crash that not only guarantees you will be smarter than whenst you started it, but chicks will dig you too.

These traits (and others that have escaped my mind) is what makes money MONEY. It is not necessarily the physical atoms that make an item an excellent candidate for money, but other traits that make it a good currency of exchange.

Ergo, the question for those of you wishing to invest in something to avoid a collapsing dollar, but can't afford gold, is what things can you buy that have those same traits, but doesn't cost $1,400 an ounce?

Well, here are a couple ideas from the ole Captain;

1. Bullets - I do not mean this in a "prepare for the collapse of society type way" (although they would definitely come in handy), but they are the perfect candidate for money. They are divisible. They have intrinsic value (you can shoot prey with them). They store well. And if times get super bad everybody would certainly accept them more than gold bracelets. Even if times AREN'T super bad, you can sell them for more when inflation goes up 50% next year because the bullets have value, Obama-dollars don't.

2. Booze - In the Wiemar Republic with hyperinflation running rampant, the Germans would use bottles of booze as a means of currency. A high end cognac would be the rough equivalent today of a $100 bill. Windsor Canadian would be the equivalent to a quarter. Regardless, again, the same traits. Divisibility. Store of value. Universally accepted. Intrinsic value. And if the world is in that bad of shape, how COULDN'T booze be in higher demand?

3. Salt - This would be more along the lines of "oh crap, the world really is collapsing." Good news is you can stock up for free essentially at restaurants by stealing salt packets.

4. Matches - Come on! Tell me how matches aren't the perfect money? AND FREE TOO! Of course if the economy doesn't DESTROY itself, then people will look at your fine match collection and say, "What, are you kidding me? I can get matches for free at the bar." But when the economy does collapse, and the lefties have shut down all the sulfur mines due to environmental concerns, boy, tell me that isn't going to be a great investment! Not to mention who are the ladies going to want to cuddle up with? Thor, the wise and mighty economist who saved up matches and has a nice warm hut, replete with roaring fire and a full arsenal of guns to protect his compound? Or Jayden, the sensitive 90's man who majored in philosophy and is now an icicle in breadline at some government feed station along with the rest of the losers who shut down the sulfur mine?

5. Tools - If you get a good set of tools think about how great that is. YOu only need one set of good tools to repair the Mad Max car you have to fight off the roving bands of marauders. But you could sell a wrench or a screwdriver for BILLIONS of Obama-dollars come 10 years from now. Regardless, tools do keep their value and are something that does have intrinsic value and would definitely be something that would hold its own against inflation.

I'm sure there are more, and if you think about it, you'll start to see them. But in the meantime if you can't afford yourself some gold, I'm sure you can afford yourself some of the items above.

This public service announcement brought to you by Cappy Cap.

I Shall Name My Child "Thor"

Honest to $#*&%#(* Christ.

You just can't make it up.

ht

From a reader who picked something I skimmed over.



Honest to )(#@$#&)(*#$@___#@#$&#$# Christ. "lactation consultant?"

Notice the hyphenated name.

I'm outta here.

Enjoy the decline.

Hyperinsulinemia and Anorexia?

In the course of a discussion over at Jimmy Moore's forum I came across something I did not know.  Anorexics -- the thinnest among us! -- can also become hyperinsulinemic!!!!   How can that be??  

If it's all about the insulin causing fat accumulation, one would think this condition would result in any dietary intake getting trapped in the fat tissues, making it unavailable to the anorexic for fat-burning, resulting in voracious hunger.  

But we would expect the anorexic to have very low postprandially-induced insulin levels.  No matter what they eat, they don't eat much.  So, where is this insulin coming from?  

It would seem to be, yet again, a defense mechanism of our bodies.  I've come across quite a bit of contradictory observations on this.

For example, in this article, anorexics had lower postprandial insulin responses and higher metabolic rates of insulin clearance and describe anorexia as being associated with improved insulin sensitivity.  They also have decreased basal insulin levels.  The authors propose this is an adaptive mechanism to protect the anorexic from hypoglycemia.  Here is another article describing improved insulin sensitivity in anorexia.  The hormonal levels from that study are shown below.

However searching on hyperinsulinemia and anorexia yields some interesting hits:

Hyperinsulinemia; a mediator of decreased food intake and weight loss in anorexia nervosa and major depression.

A brief review is made of the role of insulin in satiety and in the control of body weight, and of the newly available techniques to accurately quantify secretion, hepatic extraction, and post-hepatic delivery rates of insulin. Neural, metabolic, and endocrine stimuli affect insulin secretion. The hypothesis is therefore compatible with several etiologic factors leading to hyperinsulinemia in anorexia nervosa and major depression, and resulting in decreased food intake and weight loss.

There's also this case study (can't find anything of this paper)

How does the hyperinsulinemia develop?  Usually it's from insulin resistance, and IR would seem to be a reasonable physiological adaptation to starvation -- so as to preserve glucose for the tissues that need it most.    Elevated cortisol that is associated with anorexia could be the cause.  Perhaps the changes in insulin sensitivity are time/progression dependent, with one occurring early on, the other developing later?

Still, it is interesting that the elevated insulin is associated with further REDUCED intake, not vice versa.  

We Don't Need No Stinking "Fathers"

This is the tragic and sad result of a fatherless world.

Enjoy the decline!

Your Recession Medicine

GCBC Reference Check ~ Part III of ? ~ Is glycerol phosphate rate-limiting?

In his most recent interview with Jimmy Moore, Gary Taubes did a bit of a mea culpa on the notion that dietary carbs are required to store fat.   He offers up a rather weak description of how he got it wrong for so long in his lectures ("skewed") and claims this wasn't something from the book but rather the lectures. Originally my post here stated that strictly speaking this was true, but upon rereading those sections of GCBC it is quite obviously not.  One could even go so far as to say it is the lynchpin of his hypothesis, but that is open to interpretation.  Still, Taubes repeated in the interview that G3P is "rate limiting" in the esterification process, a claim he made unequivocally  in GCBC.  Here's the relevant paragraph:

A single molecule plays the pivotal role in the system.  It goes by a number of names, the simplest being glycerol phosphate.  This glycerol-phosphate molecule is produced from glucose when it is used for fuel in the fat cells and the liver, and it, too, can be burned as fuel in the cells.  But glycerol phosphate is also an essential component of the process that binds three fatty acids into a triglyceride.  It provides the glycerol molecule that links the fatty acids together. †116  In other words, a product of carbohydrate metabolism -- i.e., burning glucose for fuel -- is an essential component in the regulation of fat metabolism: storing fat in the fat tissue.  In fact, the rate at which fatty acids are assembled into triglycerides, and so the rate at which fat accumulates in the fat tissue, depend primarily on the availability of glycerol phosphate.  The more glucose that is transported into the fat cells and used to generate energy, the more glycerol phosphate will be produced.  And the more glycerol phosphate produced, the more fatty acids will be assembled into triglycerides.  Thus, anything that works to transport more glucose into the fat cells -- insulin, for example, or rising blood sugar -- will lead to the conversion of more fatty acids into triglycerides, and the storage of more calories as fat.

In his footnotes, Taubes cites the following book:  Regulation in Metabolism by Newsholme & Start, 1973.  Here are two of the citations because I think their wording would indicate that Taubes feels this text is authoritative, and, presumably if he's recommending it, he has read it himself. 

An excellent review of the regulation of fat metabolism and adipose tissue is Newsholme and Start 1973:  195-246.

Glycerol phosphate:  For a review of the role of this molecule, the triglyceride/fatty-acid cycle, and the glucose/fatty acid cycle, see Newsholme and Start 1973:214-34.

OK, so I did go "see" for myself.  I've been somewhat sitting on this one for a while because I think it is particularly damning given specific wording of the excerpts from this text I'm about to share.   I wanted to share it first in my interview with Jimmy (even though that won't air for a few months).

What I transcribe below is the section in Chapter 5 Adipose Tissue and Fat Metabolism entitled "The control of esterification" that deals with this theory:  {} are my comments ;-)

In the case of the hypothetical, primitive animal it has been shown how large changes in blood glucose concentration could automatically cause reciprocal changes in plasma fatty acid concentration.  However, in the rat the blood glucose concentration does not fall by more than 30% during two days of starvation and this would appear to be insufficient to cause the marked increase in fatty acid mobilization that occurs under these conditions.  During the same period the plasma insulin level is decreased by about 80% (ref 41, see Table 7.3) and this hormone is known to regulate esterification.  Insulin stimulates the membrane transport of glucose into the adipose tissue cell and increases the rate of glycolysis and the glycerol phosphate concentration.  During starvation the reduction in the plasma insulin level results in a decreased rate of glycolysis and a lowering of the glycerol phosphate concentration.  This restricts esterification and consequently fatty acid mobilization is stimulated.   {I know what you're thinking ... so far so good right?} 

This theory is supported by the fact that the content of glycerol phosphate in adipose tissue is decreased during starvation and it is markedly increased when adipose tissue from a starved animal is incubated with glucose and insulin.  {Here is where I believe, having heard all he needed to hear, Taubes stopped reading ... but read on dear readers}   There are a number of problems associated with the simple idea that esterification is controlled by the membrane transport of glucose.  First, there is no evidence that the concentration of glycerol phosphate is limiting for the process of esterification (the Km for glycerol phosphate of the first enzyme in the pathway is not known).  Second, since glycerol phosphate dehydrogenase catalyses a reaction which is close to equilibrium, the concentration of glycerol phosphate can be controlled by both the cytoplasmic [NAD+]/[NADH] ratio and the concentration of dihydroxyacetone phosphate. (ref 42)

Dihydroxyacetone phosphate + NADH ↔ Glycerol phosphate + NAD+   

These quantities may vary independently of the glycolytic rate. (ref 17)  Third, the addition of adrenaline, fatty acids or acetate to the incubated fat pad preparation stimulates esterification but does not increase the content of glycerol phosphate. (ref 42)  This experiment suggests that factors other than the glycerol phosphate concentration can regulate esterification.  Such factors remain unidentified at present.  Nonetheless, it must be emphasized that a marked decrease in the concentration of glycerol phosphate could limit the rate of esterification and therefore variations in its concentration must always remain a potential mechanism of control.

The entire first paragraph essentially lays out a hypothesis, and evidence consistent with that hypothesis is included in the opening sentence of the second.  But the gist of the remainder of this paragraph is to lay out the case AGAINST it.

I don't know how much more bluntly Newsholme and Start could have stated the first point.  To repeat:  

"there is no evidence that the concentration of glycerol phosphate is limiting for the process of esterification."

Just how does one go from that to:

In fact, the rate at which fatty acids are assembled into triglycerides, and so the rate at which fat accumulates in the fat tissue, depend primarily on the availability of glycerol phosphate.

???????????????????   You'll note I'm picking at Taubes' wording here too.  He uses that word fact, not probably, not "could", not that this is some conjecture etc.

The second point is really the biggie here.  Let me try to explain this to those without a degree in chemistry.  All chemical reactions can theoretically proceed in either direction, so that if A + B → C + D, then C + D → A + B.  Many chemical reactions are considered irreversible because one direction is much more energetically favorable than the other.  The energy requirement to go in reverse is simply too high.  Combustion of hydrocarbons is a good example (e.g. burning propane).  But other reactions can go in both directions, we call these reversible reactions, and use the double arrow to indicate this (actually it's usually two arrows in opposite directions on top of each other, often with the length of the arrows reflecting the preferred direction).     If we put compounds A&B, C&D, or three or all four of them into a beaker, initially one reaction occurs at a faster rate but both are occurring until the system reaches a state of equilibrium.  At equilibrium, the concentrations of A, B, C, and D remain constant, and we can define an equilibrium constant (Keq) that represents a ratio of these concentrations.  This makes the system appear static, but it is actually a dynamic equilibrium with the rates of the forward and reverse reactions being equal.  There is a principle called LeChatelier's Principle that applies to systems in equilibrium.  In short, if we do anything to displace the system from its equilibrium state (in chemistry we usually referred to this as perturbing the equilibrium or applying a stress), the reaction rates will temporarily "shift" in order to re-establish the equilibrium.  One way we can do this is to add one or more of the compounds to the system.  The equilibrium constant Keq is called a constant for just that reason.  If I add more A to the system above that is at equilibrium, I have increased the concentration of A and thus altered K (which is a ratio of the concentrations).  The system will react so as to lessen the concentration of A so as to bring K back to Keq.  This would involve a "shift to the right" being an increase in the reaction rate of the forward reaction.  (If you're interested in the math involved, here's one example).

So what they are saying in the second point is that the

DHAP + NADH ↔ GP + NAD⁺ 

reaction is close to equilibrium and therefore should behave in the manner described above.  If we add DHAP then GP formation should increase.  If there's more NADH, it should as well, and if there's more NAD⁺ then the reverse reaction should "consume" GP and reduce its concentration.  But the concentrations of these other three components of the equilibrium system vary in ways that are not correlated with how much glycolysis is going on.  Were this system controlled simply by LeChatelier's Principle, then increases in DHAP (an intermediary in glycolysis) would exert predictable changes in the other three components of this system.  Rather, the conversion of DHAP to GP is determined by the activity of an enzyme.

On to point 3 that directly addresses whether it is the G3P level (however manipulated) that is rate limiting in esterification.  The addition of adrenaline, fatty acids OR acetate alone can increase esterification rate without a corresponding increase in the G3P level in the cell.   Of course at the time of publication, the text states that the mechanisms of this were not yet known.  I suspect ASP is working it's magic here.  The lack of change in G3P level indicates two possibilities, either basal G3P levels are in sufficient excess of needs that whatever stimulates esterification only depletes the G3P slightly as it is incorporated into triglycerides, or fatty acid uptake (or adrenaline or acetate) stimulates G3P production to meet the needs to esterify FA's but the additional G3P is consumed in the esterification process so that the level remains unchanged, or both.

Bottom line:  This reference DIRECTLY contradicts that which Taubes cites in GCBC and implies is discussed in this text.  At a minimum, Taubes should have done what he says he does  and follow the research forward to present day.  That there were factors unknown in 1973 should have led him to further research and no doubt to discover ASP.  But he clearly didn't want to.  

Throughout this process, I necessarily made judgments about the quality of the research and about the researchers themselves.  I tried to do so using what I consider the fundamental requirement of good science:  a relentless honesty in describing precisely what was done in any particular work, and a similar honesty in interpreting the results without distorting them to reflect preconceived opinions or personal preferences […]  I hope that I, too, will be judged by the same standard.    

~ Gary Taubes in Good Calories, Bad Calories

Just doing my part here.  Taubes' continued silence on these matters "speaks volumes".

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If this comment remains here, it means that to date that you are reading this post, Gary Taubes has not formally addressed this very real criticism and issue with his writings.  He has also failed to set the record straight in any meaningful forum which is why you still have people claiming, to this day, that you can't store fat or get fat without dietary carbohydrate.