Monday, May 31, 2010

I Do Care Who Started It

And these peaceniks would NEVER EVER start something now would they?

Glyceroneogenesis v. Taubes

My greatest criticism of Taubes is that despite several years of "exhaustive" research, and a deluge of references in his book, the bulk of his "Adiposity 101" is either unreferenced, or based on decades old physiology texts and papers.

In this lecture (Slide 48 at around 46 min in) is his discussion of glycerol-3-P.  Taubes is a master of stating facts ... in a misleading way that (1) leads the listener/reader to incorrect conclusions, and (2) enables Taubes to use the "I never said that" out when challenged.

He first quotes a 1970's text on the Fatty Acid Cycle and shows an updated text of similar.  In both he highlights the need for glycerol-3-P to esterify FFA's to triglycerides.  This is true.  

However on Slide 48 he presents a bunch of cobbled together "facts" that are either not considered settled science or are taken out of context.  And I note that while he now (2009) lists glyceroneogenesis on his slide, the word never passes his lips.  He jumps right over this bullet point on the slide!!   I cannot help but think that he has been informed since the 2007 publication of his book that such a metabolic path exists.  But since acknowledging it would probably require scrapping this entire section of his lecture and derail his money train, he prefers to include a term on a slide in a long lecture and hope nobody notices.  Since this is a term few if any have a clue about, he's successful, and anyone who is reading his slides is likely to take at face value  his assertion that it is only a small amount.  If not outright deception in the name of financial gain, Taubes is at the very least displaying a degree of willful ignorance.

But maybe this whole glyceroneogenesis stuff is too recent to address, so Taubes is just relying on the old info b/c nothing concrete has come about.  Well, in addition to the comprehensive overview of the Fatty Acid - Triglyceride Cycle including glyceroneogenesis (2003), I recently came across this:

Glyceroneogenesis comes of age  2002

The science of glyceroneogenesis was being elucidated around the time that, presumably, Taubes began his lengthy research efforts following his Big Fat Lie NYT article.  How did he miss all of this?  And how, in 2009 can he continue to ignore this.

As I've blogged on previously,  the low carb nutritional state mimics the fasted state.  There is no reason to believe that the processes upregulated similarly for fasting and LC "fed" (gluconeogenesis, increased ketone formation, etc.) state would exclude glyceroneogenesis.  Indeed there is every indication that they are.

UPDATE:  It just got worse as I got my Sony ebook software working again to search GCBC for glyceroneogenesis.  Well, it's nowhere in the text, but it is right there in the title of one of his references.  The 2003 article linked to above.  I'm left to conclude this man is totally bereft of intellectual honesty.  
Live Cockroaches Crawling On My Face Part 2

Filming a scene from the book Hard Time yesterday.
Link to video at YouTube.

Tags: cockraoches jail prison phoenix arizona sheriff joe arpaio shaun attwood hard time inmate prisoner human rights maricopa county insects cell police cops guards jon's jail journal blog
Live Cockroaches Crawling On My Face Part 1

Filming a scene from the book Hard Time yesterday.
Link to video at YouTube.

Tags: cockraoches jail prison phoenix arizona sheriff joe arpaio shaun attwood hard time inmate prisoner human rights maricopa county insects cell police cops guards jon's jail journal blog
Hard Time Internet Banner Number 2

My friend, Stephanie, made this banner, which links to where is selling Hard Time: A Brit in America's Toughest Jail. There are now less cockraches on the book cover, but also a larger more detailed one.

Click here for the code if you want to use this banner at your website.

Sunday, May 30, 2010

Sudden Cardiac Death and Free Fatty Acids

Here is the Heart Rhythm Society's Definition:
Sudden cardiac death (SCD), also called cardiac arrest, is used to describe a situation in which the heart abruptly and without warning stops working, so no blood can be pumped to the rest of the body. It is responsible for half of all heart disease deaths.
Sudden cardiac death occurs when the heart’s electrical system malfunctions. It is not a heart attack (also known as a myocardial infarcation). A heart attack is when a blockage in a blood vessel interrupts the flow of oxygen-rich blood to the heart, causing heart muscle to die. So if the heart can be compared to a house, SCD occurs when there is an electrical problem and a heart attack – when the problem is the plumbing.
Later in that summary it is stated that 75% showed evidence of prior heart attack, and 80% evidence of CVD.  So that leaves 25% with no evidence of prior heart attack and 20% with no CVD.

So I do a little math:
*  SCD deaths occurring in people with no prior cardiac event that caused discernible damage to heart:
                 (0.5 of all CD's are SCD's) *( 0.25 no prior heart attack) * 100 = 12.5%
                 That's one out of every eight.
* SCD deaths occurring in people with no evidence of CVD
   (presumably athersclerosis/blockage/etc. but could also include other heart problems):
                 (0.5 of all CD's are SCD's) *( 0.20 no evidence of CVD) * 100 = 10%
                 That's one out of every ten.

So why do I care about this?  Because the one thing that is most predictive of SCD is elevated free fatty acids (NEFA/FFA), a characteristic of Metabolic Syndrome, Diabetes (Type I & II) ... and VLCD!!  While many with pre-diabetes/IR/Type II successfully use carbohydrate restriction to successfully control blood glucose levels,  this can be at the expense of further elevation of circulating free fatty acids.  A high fat, low carb meal can have the effect on NEFA/FFA levels that a high carb meal would have on blood glucose.

1.  Elevated plasma free fatty acids predict sudden cardiac death: a 6.85-year follow-up of 3315 patients after coronary angiography
Aims Sudden cardiac death (SCD) is the most common fatal cardiovascular event. Free fatty acids (FFAs) exert several harmful effects on the myocardium and may therefore contribute to SCD. We examined whether fasting FFA predict SCD in patients who had undergone coronary angiography.
Methods and results FFAs were measured at baseline (1997–2000) in 3315 patients scheduled for coronary angiography. Angiographic coronary artery disease was found in 2231 study participants. {My Note: Although this study was in men referred for angiography, roughly 1/3rd were FREE of coronary artery disease}.  After a median time of follow-up of 6.85 years, 165 SCD occurred in the entire study population. In a Cox proportional hazards model, the unadjusted hazard ratio (HR) for SCD in the fourth when compared with the first FFA quartile was 2.95 (95% CI 1.84–4.73; P < 0.001). After adjustment for common and emerging cardiovascular risk factors, the HR remained significant at 1.76 (1.03–3.00; P = 0.038). High FFA levels were also significantly associated with all-cause and cardiovascular mortality, even after exclusion of patients with SCD.
Conclusion Our study shows that elevated plasma FFAs are an independent risk factor for future SCD in patients referred to coronary angiography. These results may suggest that modulation of myocardial fatty acid uptake and/or metabolism are a possible target of treatment, but it still remains to be clarified whether high FFA levels are a cause or a consequence of pathological processes that underlie the association between FFA and SCD.


Circulating Nonesterified Fatty Acid Level as a Predictive Risk Factor for Sudden Death in the Population

{My Note:  This study separately analyzes a subset of data from the Paris Study where no ischemia was found}
Background— In ischemic conditions, concentration of circulating nonesterified fatty acids (NEFA) is increased and has a proarrhythmic effect that is responsible for ventricular tachyarrhythmias. In nonischemic patients, high NEFA plasma concentration has been shown to be associated with frequent premature ventricular complexes and increased familial risk of cardiovascular disease, but its relation to sudden death has not been studied. We assessed the role of circulating NEFA in sudden death in asymptomatic men in a long-term cohort study.
Methods and Results— A total of 5250 men employed by the city of Paris, aged 42 to 53 in 1967 to 1972, free of known ischemic cardiac disease, and included in the Paris Prospective Study I, completed a second annual examination and had fasting plasma circulating NEFA measured. Each subject underwent a physical examination and ECG, provided blood for laboratory tests, and answered questionnaires administered by trained interviewers. Vital status was obtained for each subject from specific inquiries until he retired; after retirement, it was obtained from death certificates. Body mass index, systolic and diastolic blood pressures, tobacco consumption, parental history of sudden death, fasting cholesterol level, and circulating NEFA concentration were independent factors associated with sudden death during follow up (average, 22 years). When adjusted for confounding factors, circulating NEFA concentration remained an independent risk factor for sudden death (relative risk, 1.70; 95% confidence interval, 1.21 to 2.13) but not for fatal myocardial infarction.

Conclusions— Circulating NEFA concentration is an independent risk factor for sudden death in middle-aged men. Some form of primary prevention could be envisaged in subjects at high risk of sudden death.

These two articles contain a LOT of background in their full texts.  A lot of it is disturbing.  I won't copy all of it here, but some summaries.  If you click on my links to the free full text, you can follow active links to referenced studies, etc.

From #1:

Circulating FFAs are mainly released from triglyceride stores of the adipose tissue and serve as physiologically important energy substrates. An excess of FFA has been implicated in insulin resistance and hepatic steatosis.3,4 Furthermore, elevated FFAs are associated with atherosclerosis5 and hypertension.6 Fatty acid oxidation supplies the heart with ∼70% of its energy but an overwhelming delivery of plasma FFA to the heart, as it is observed in acute coronary syndromes (ACS) and heart failure, may contribute to myocardial dysfunction.2,7,8 High FFA and subsequent increased utilization of fatty acids for energy generation in the ischaemic myocardium may cause a ‘metabolic crisis’ in patients with CAD because fatty acid oxidation requires more oxygen when compared with the use of glucose.2,7 Apart from this, high concentrations of FFA have been shown to exert pro-arrhythmic actions.2,9,10
This study's results:  Note 1st Quartile = Fourth of subjects with lowest NEFA on up to the 4th Quartile containing the fourth of subjects with the highest NEFA levels.

I could copy the entire discussion from reference 2, but instead here's a direct link to that section:

Why does this concern me?  Well, I'm otherwise healthy, but when I ballooned up to the 260's-270's after my first stint on LC, I (not immediately, but when I was that weight for a while) developed a racing heart w/o exertion, listed as a risk factor in my first link.  This occurred sometimes in my sleep to the extent that the pounding of my heart in my ears woke me up!  After my second stint on LC I had the racing heart with relatively mild exercise -- I was in the low 200's at the time and feeling and looking pretty great at the time (I weigh more than I appear to).  Now I had a bunch of tests run that ruled out heart abnormality and wore a Holter monitor and even experienced a related symptom while wearing that.  My heart didn't skip any beats, and I've never had an abnormal EKG, but still ... every now and then, even now.

When one looks at fasting lipids, there is always the question of whether it is the circulating lipids themselves that are "causing" something, or if they are merely a symptom of underlying metabolic imbalance, some other factor or factors of which actually cause disease.  Fasting triglycerides are an example of this.  By now most have seen the differing triglyceride profiles of high carbers vs. low carbers, and excessive carb consumption does lead to elevated fasting trigs.  But most of the fat low carbers consume do not exist as trigs, and clearance of triglycerides from the blood has been shown to be faster (this makes sense, we're fat adapted).  Still ... is it the triglycerides themselves that exert a directly damaging effect?  Or is it that residual trigs indicate a metabolic imbalance?  Many of the references for NEFA seem to point to the fact that it is the LEVEL OF THESE IN CIRCULATION that is associated with negative implications or that can elicit a problem in an otherwise healthy animal/human.  A HF/VLC diet offers a double assault on NEFA levels.  Low insulin (the crown jewel of LC'ers) levels fail to suppress lipolysis, the major source of NEFA, although dietary fats contribute some.  I think this is something we should not be so quick to ignore when considering the benefits and risks of carbohydrate restriction.

Saturday, May 29, 2010

Spontaneous Caloric Reduction with LC Diet

This study is cited in the Westman,'s LC Nutrition & Metabolism

Effect of a Low-Carbohydrate Diet on Appetite, Blood Glucose Levels, and Insulin Resistance in Obese Patients with Type 2 Diabetes

(The full text is not supposed to be free, but through this link I was able to access it as a "patient", if it doesn't work for you, ask in the comments and I'll be glad to email you the PDF I saved)

Although this is a relatively short and small study, it demonstrates what many in the LC community are strangely averse to acknowledging -- that LC leads to a spontaneous caloric restriction in most low carbers.  These folks restricted their caloric intake by an average of just over 1000 cal/day (median around 750).  Here are the dietary differences:

Before:  Carb intake ranged from 182g/day to a whopping 552g/day and averaged just over 300g/day.  
After:  Carb intake ranged in a ketogenic range of 14-32g and averaged 21g/day -- VLC
The difference, an average of around 280 g carb/day corresponds to 1120 calories.  

What I found really interesting is the corresponding fat and protein intakes.  I expected protein intake to increase dramatically, but average intake increased only 14g/day (looking at the difference column, these were the differences for each patient then averaged, so there were presumably participants that decreased their protein significantly (one by a fairly sizable 64g).  Perhaps this was the person who was consuming that whopping 552g carbs at onset?  In any case, as stated by Westman, in their LC Nutrition & Metabolism review,

Whereas instruction in an LCD does not mention calories, the restriction of dietary carbohydrate leads to a reduction in caloric intake from baseline. The ad libitum intake can vary from person to person, but, in many cases, the protein and fat intakes, in absolute terms, are not much higher than those of a typical American diet, because thetotal caloric intake is lower. As such, the LCD is not necessarily a high-protein diet or a high-fat diet. 
This was born out by this study.  On average, the participants did not replace carbs with fat or protein to any great extent.  So percentage-wise their diets were higher in protein and fat, but absolute consumption-wise, they were not raised significantly in either macronutrient.

Usual Diet:  fat+protein accounted for 1934 cal, 28% protein/72% fat
LC Diet:  fat+protein accounted for 2080 cal (only 150 cal combined increase), 29% protein/71% fat

Also, even in the short term, this study did NOT demonstrate any so-called metabolic advantage.

Before The New Atkins

Westman, Volek and Phinney were among the contributers (and Westman headlined) the following, partially Atkins Foundation funded, review:

Low-carbohydrate Nutrition and Metabolism

I can't recommend reading this highly enough.

I've listed the references in a separate post, numbered (the formatting farkled the last few but I'll let you count ;) )

For a non-gimmicky discussion of how low carb diets REALLY work for weight loss, this is where it's at!

Paleolithic Nutrition -- Eaton 12 yr. Update

Paleolithic nutrition revisited: A twelve-year retrospective on its nature and implications

Friday, May 28, 2010

Big Oil vs. Big Banks

I'll send somebody a shinny new nickel if they can explain to me that when BP screws up we make sure they pay every dime in damages, but if a bank screws up we bail them out with taxpayer money.

Rita Wilson

I love how they use children to extort money from the taxpayer.

Yes, won't somebody please think of the children.

Another question is would you really want this woman teaching your child in any subject, simply because what kind of warped ethics would she be teaching them?

Steve Wynn

My new hero.

Of the many things I like in it those that I like the most;

1. He's essentially shorting America by investing in its vices. Spend money you don't have, sex, live for the moment. He'll be the one with the cash after it's all said and done.

2. He finds it easier to deal with the Chinese government than the US government.

3. His quip on EBITDA. EBITDA, for those of you without the benefit of an accounting degree is your "Earnings Before Interest, Taxes, Depreciation and Amortization."

This measure is basically the most liberal and handicapped measure of a company's profits because (as far as lenders are concerned) this is the amount a company has to pay any loans that are made to it - the money you have before you pay out interest, taxes and account for depreciation and amortization.

I've never liked the concept of depreciation and amortization. I do understand the "matching" principle of accounting in that you spread out the cost of long term fixed assets to match the overall expense with the revenue it helps generate over the years, but for larger companies that are always buying fixed assets to replace the old ones, would simply expensing your purchases outright really make any difference between your cash flow and net income.

I also have a distaste for EBITDA because it was always used by bankers as the measure to see how much debt a company could afford. LITERALLY ignoring the fact the company would have to spend some money SOMETIME in order to keep its operations going. So if you based your loan on the amount EBITDA showed, you were pretty much guaranteed to be lending beyond the payback capacity of the borrower.

Alas, it was these sort of "rocking the boat" observations that attracted the criticism of my now insolvent previous employers, but as Steve Wynn has pointed out the "City Center" project which was financed by the likes of my previous employers, is belly up and bankrupt.
Question Time with 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, the accomplices can get 25-year sentences.

Leigh asked these questions:

Is there work for everyone who wants to work?

No. Although the policy states, “Every inmate shall work,” the reality is that jobs are quite scarce here. I estimate that around 40% of us are employed. Some of these are “paper jobs” in that they only exist on paper. Most of the guys would love a job, as otherwise they’re cooped up in the dorms all day with all of the other unemployed. All that restless energy and free time translates itself into mischief and noise and discontent. I count myself extremely fortunate to have such a good job! By contrast, I’ve just started a series of posts about my first prison job way back in ’94 about cleaning up blood and feces for a nickel an hour!

What changes have you seen (if any) since the economy has gotten even worse?

They have been steady. First, everyone’s wages went down by a nickel. Then our work hours got rolled back from 80 a week to 60 or less. The most dramatic change will occur this April. They circulated a memo stating that they can no longer afford to feed us dinner. Yes, seriously! Instead, we’ll receive the gut-meat sack meal I described in “A Doomed Sock.” Even more amazing was the gall of the director’s remark in that memo: “The quality of the meals will not change.” C’mon now, that’s just insulting!


Now, I hear some of you thinking, “You ungrateful so-and-so! They should only give you bread and water.” Hey, I understand. I really do. Not everyone here has evolved out of deserving to be here. Despite my bias towards prisoners rights, there are a lot of guys here I don’t like, I avoid, and who will undoubtedly come right back. But the reality of it is, every person here is an individual. Lumping us all into a convenient stereotype is just as short-sighted as a racial slur. Yeah, some of us may be incorrigible or dope fiends or whatever. But some of us aren’t. I’ve taken full responsibility for my crimes since I turned myself in back in 1993 and confessed. I expect no sympathy – or hero worship as someone put it! – just a chance to be heard as an individual in 2010, and not forever judged by one mistake 17 years ago.
Thus endeth the sermon!

Click here for Polish Avenger’s previous Question Time.

Our friends inside appreciate your comments.

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

Shaun Attwood

Thursday, May 27, 2010

The Bachelor Budget

Many years ago, when the Captain was but a wee private, he put himself through college working at the campus police department doing campus security. It paid $6.90 and after three years and several promotions he was making $9.10 per hour.
I worked full time while going to school full time, but not once did I ever make more than $20,000 in any given year. However, I didn't need to, because by the end of my college days I had a surplus of $6,000 (which I bought a converitble with to celebrate finishing college). And while there has no doubt been inflation over the past 15 years, this spartan existence behooves the question;

"What is the absolute minimal amount a single person can live on today?"

I ask the question because whereas 15 years ago your young and naive Captain had dreams of working hard and establishing a long and successful career, observations of mortality and a limited life starts to make one think how does one spend their finite time on this planet. You throw in a recession, a-soon-to-be overall tax rate of 40%, the increasing likelihood Roth/401k's/IRA's will be rescinded and nationalized, and a general deteriorating future for the country it's like being the navigator on the Titanic. Inevitably you should give up trying to convince the captain to change course and just pony up to the bar and get the finest bottle of scotch.

Thus some back-of-napkin calculations to find out what, if necessary, is the absolute minimal a single person can live off of and pursue a life of leisure fully intending to maximize their free time on this planet and not to build up an estate or empire.

My estimate is in today's dollars $16,200 in annual income should cover every bachelor's basic desires and needs. This of course assumes several things;

1. Never a new car, always used.
2. Liability insurance only
3. No children
4. Catastrophic insurance only
5. No traditional "$25,000" wedding should he/she get married.
6. Living in an area that is NOT New York or San Francisco or some other expensive area to live
7. Roomate or a cheap one bedroom apartment

Now I am being serious here because I want to make sure I've caught everything. Do any of the Cappy Cap readers see something in my budget that is missing? The reason for my adamancy is because if we can calculate a precise number, then it will allow people to look at their personal finances, see if they can live on that amount, and if so, then weigh whether a life of slaving away for $60,000, $35,000 net, not to mention the standard corporate political BS that comes with it and complimentary high blood pressure and 2 hour commute, is a better existence than working some night time security job for $18,000 a year and fishing and reading books.

"Where are We Going?"

A colleague of mine asked and I thought this e-mail might be of some humor and entertainment;

Without going into detail, I predict a general decline ala Japan from 1989 to today. YOu will see the "Herbivore" movement in Japan come to the US and (gender politics set aside) men just frankly leave their traditional roles which will have large implications for future economic growth as well as stagnation in corporate profits and thus stock prices. This decrease in economic growth, combined with a decrease in asset prices is going to impair and underfund not just private pensions, but 401k's IRA's and 457's. Spending commitments made by Obama will essentially make the future so uncertain and taxes so likely that everybody, regardless of gender, will be less incented to work. Productive, hard working people who would have normally bred future generations of workers will opt for vasectomies instead and choose a life of leisure over work. This will bode ill for current and future pensioneers who were relying upon others to essentially work for them and pay for their retirement, not to mention health care. Nothing will change until the younger generations get a rude awakening that "unfortunately, yes little Jimmy, you do actually have to produce something of value in order for society to succeed, let alone, survive," but this lesson will be delayed as the rest of the world panics and throws money into the US dollar as a flight to safety simply because its "the US" permitting us to borrow more money and live the Barbie World lifestyle where we produce nothing, but buy everything as if the US was one big shopping mall. Financial crisis inevitably ensues, Keynesian fiscal stimulus never works, economy collapses and now people will finally have the free time to study economics and figure out how we got there in the first place because nobody will have jobs.

And everybody will blame Bush.

Low-Carbohydrate Nutrition and Metabolism References

''.          Eaton SB, Konner M. Paleolithic nutrition: a consideration of its nature and current implications. N Engl J Med 1985;312:283–9.[Medline]

2.          Eaton SB. The ancestral human diet: what was it and should it be a paradigm for contemporary nutrition? Proc Nutr Soc 2006;65:1–6.[Medline]

3.          Hildes JA, Schaefer O. The changing picture of neoplastic disease in the western and central Canadian Arctic (1950–1980). Can Med Assoc J 1984;130:25–32.[Abstract]

4.          Schaefer O. The changing health picture in the Canadian North. Can J Ophthalmol 1973;8:196–204.[Medline]

5.          Shephard RJ, Rode A. The health consequences of "modernization": evidence from circumpolar peoples. Cambridge, United Kingdom: Cambridge University Press, 1996.

6.          Trends in intake of energy and macronutrients—United States, 1971–2000. MMWR Morb Mortal Wkly Rep 2004;53:80–2.[Medline]

7.          Bravata DM, Sanders L, Huang J, Krumholz HM, Olkin I, Gardner CD. Efficacy and safety of low-carbohydrate diets: a systematic review. JAMA 2003;289:1837–50.[Abstract/Free Full Text]

8.          Westman EC, Mavropoulos J, Yancy WS Jr, Volek JS. A review of low-carbohydrate ketogenic diets. Curr Atheroscler Rep 2003;5:476–83.[Medline]

9.          Larosa JC, Fry AG, Muesing R, Rosing DR. Effects of high-protein, low-carbohydrate dieting on plasma lipoproteins and body weight. J Am Diet Assoc 1980;77:264–70.[Medline]

10.      Cahill GF Jr. Starvation in man. N Engl J Med 1970;282:668–75.[Medline]

11.      Krieger JW, Sitren HS, Daniels MJ, Langkamp-Henken B. Effects of variation in protein and carbohydrate intake on body mass and composition during energy restriction: a meta-regression. Am J Clin Nutr 2006;83:260–74.[Abstract/Free Full Text]

12.      Volek JS, Sharman MJ, Love DM, et al. Body composition and hormonal responses to a carbohydrate-restricted diet. Metabolism 2002;51:864–70.[Medline]

13.      Boden G, Sargrad K, Homko C, Mozzoli M, Stein TP. Effect of a low-carbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes. Ann Intern Med 2005;142:403–11.[Abstract/Free Full Text]

14.      Harber MP, Schenk S, Barkan AL, Horowitz JF. Alterations in carbohydrate metabolism in response to short-term dietary carbohydrate restriction. Am J Physiol Endocrinol Metab 2005;289:E306–12.[Abstract/Free Full Text]

15.      Bisschop PH, De Sain-Van Der Velden MG, Stellaard F, et al. Dietary carbohydrate deprivation increases 24-hour nitrogen excretion without affecting postabsorptive hepatic or whole body protein metabolism in healthy men. J Clin Endocrinol Metab 2003;88:3801–5.[Abstract/Free Full Text]

16.      Bisschop PH, Pereira Arias AM, Ackermans MT, et al. The effects of carbohydrate variation in isocaloric diets on glycogenolysis and gluconeogenesis in healthy men. J Clin Endocrinol Metab 2000;85:1963–7.[Abstract/Free Full Text]

17.      Bisschop PH, de Metz J, Ackermans MT, et al. Dietary fat content alters insulin-mediated glucose metabolism in healthy men. Am J Clin Nutr 2001;73:554–9.[Abstract/Free Full Text]

18.      Allick G, Sprangers F, Weverling GJ, et al. Free fatty acids increase hepatic glycogen content in obese males. Metabolism 2004;53:886–93.[Medline]

19.      Bisschop PH, Bandsma RH, Stellaard F, et al. Low-fat, high-carbohydrate and high-fat, low-carbohydrate diets decrease primary bile acid synthesis in humans. Am J Clin Nutr 2004;79:570–6.[Abstract/Free Full Text]

20.      Phinney SD, Bistrian BR, Evans WJ, Gervino E, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation. Metabolism 1983;32:769–76.[Medline]

21.      Noakes M, Foster PR, Keogh JB, James AP, Mamo JC, Clifton PM. Comparison of isocaloric very low carbohydrate/high saturated fat and high carbohydrate/low saturated fat diets on body composition and cardiovascular risk. Nutr Metab 2006;3;7.

22.      Allick G, Bisschop PH, Ackermans MT, et al. A low-carbohydrate/high-fat diet improves glucoregulation in type 2 diabetes mellitus by reducing postabsorptive glycogenolysis. J Clin Endocrinol Metab 2004;89:6193–7.[Abstract/Free Full Text]

23.      Meckling KA, O'Sullivan C, Saari D. Comparison of a low-fat diet to a low-carbohydrate diet on weight loss, body composition, and risk factors for diabetes and cardiovascular disease in free-living, overweight men and women. J Clin Endocrinol Metab 2004;89:2717–23.[Abstract/Free Full Text]

24.      Nordmann AJ, Nordmann A, Briel M, et al. Effects of low-carbohydrate vs low-fat diets on weight loss and cardiovascular risk factors. Arch Intern Med 2006;166:285–93.[Abstract/Free Full Text]

25.      Nickols-Richardson SM, Coleman MM, Volpe JM, Hosig KW. Perceived hunger is lower and weight loss is greater in overweight premenopausal women consuming a low-carbohydrate/high-protein vs high-carbohydrate/low-fat diet. J Am Diet Assoc 2005;105:1433–7.[Medline]

26.      Miller BVM III, Bertino JSJ, Reed RG, et al. An evaluation of the Atkins' Diet. Metabol Syndr Relat Disord 2003;1:299–309.

27.      Rodin J, Wack J, Ferrannini E, DeFronzo RA. Effect of insulin and glucose on feeding behavior. Metabolism 1985;34:826–31.[Medline]

28.      Holt SH, Miller JB. Increased insulin responses to ingested foods are associated with lessened satiety. Appetite 1995;24:43–54.[Medline]

29.      Valasquez-Mieyer PA, Cowan PA, Arheart KL, et al. Suppression of insulin secretion is associated with weight loss and altered macronutrient intake and preference in a subset of obese adults. Int J Obes Relat Metab Disord 2003;27:219–26.[Medline]

30.      Feinman RD, Makowske M. Metabolic syndrome and low-carbohydrate ketogenic diets in the medical school biochemistry curriculum. Metabol Syndr Relat Disord 2003;1:189–97.

31.      Silva JE. The thermogenic effect of thyroid hormone and its clinical implications. Ann Intern Med 2003;139:205–13.[Free Full Text]

32.      Cannon B, Nedergaard J. Brown adipose tissue: function and physiological significance. Physiol Rev 2004;84:277–359.[Abstract/Free Full Text]

33.      Hirsch J, Hudgins LC, Liebel RL, Rosenbaum M. Diet composition and energy balance in humans. Am J Clin Nutr 1998;67(suppl):551S–5S.[Abstract]

34.      MacLean PS, Higgins JA, Johnson GS, et al. Enhanced metabolic efficiency contributes to weight regain after weight loss in obesity-prone rats. Am J Physiol Regul Integr Comp Physiol 2004;287:R1306–15.[Abstract/Free Full Text]

35.      Bluher M, Michael MD, Peroni OD, et al. Adipose tissue selective insulin receptor knockout protects against obesity and obesity-related glucose intolerance. Dev Cell 2002;3:25–38.[Medline]

36.      Chen HC, Jensen DR, Myers HM, Eckel RH, Farese RVJ. Obesity resistance and enhanced glucose metabolism in mice transplanted with white adipose tissue lacking acyl CoA:diacylglycerol acyltransferase 1. J Clin Invest 2003;111:1715–22.[Medline]

37.      Kraemer FB, Shen WJ. Hormone-sensitive lipase knockouts. Nutr Metab (Lond) 2006;3:12.[Medline]

38.      Feinman RD, Fine EJ. "A calorie is a calorie" violates the second law of thermodynamics. Nutr J 2004;3:9.[Medline]

39.      Fine EJ, Feinman RD. Thermodynamics of weight loss diets. Nutr Metab (Lond) 2004;1:15.[Medline]

40.      Welch GR. Some problems in the usage of Gibbs free energy in biochemistry. J Theor Biol 1985;114:433–46.[Medline]

41.      Feinman RD, Fine EJ. Nonequilibrium thermodynamics and energy efficiency in weight loss diets. Theoret Biol Med Model (in press).

42.      Kabashima T, Kawaguchi T, Wadzinski BE, Uyeda K. Xylulose 5-phosphate mediates glucose-induced lipogenesis by xylulose 5-phosphate-activated protein phosphatase in rat liver. Proc Natl Acad Sci U S A 2003;100:5107–12.[Abstract/Free Full Text]

43.      Gumbiner B, Wendel JA, McDermott MP. Effects of diet composition and ketosis on glycemia during very-low-energy-diet therapy in obese patients with non-insulin-dependent diabetes mellitus. Am J Clin Nutr 1996;63:110–5.[Abstract/Free Full Text]

44.      Rizza RA, Mandarino LJ, Genest J, Baker BA, Gerich JE. Production of insulin resistance by hyperinsulinaemia in man. Diabetologia 1985;28:70–5.[Medline]

45.      Westman EC, Yancy WS Jr, Haub MD, Volek JS. Insulin resistance from a low carbohydrate, high fat diet perspective. Metabol Syndr Relat Disord 2005;3:14–8.

46.      Phinney SD. Ketogenic diets and physical performance. Nutr Metab (Lond) 2004;1:2.[Medline]

47.      Peters SJ, Harris RA, Wu P, Pehleman TL, Heigenhauser GJ, Spriet LL. Human skeletal muscle PDH kinase activity and isoform expression during a 3-day high-fat/low-carbohydrate diet. Am J Physiol Endocrinol Metab 2001;281:E1151–8.[Abstract/Free Full Text]

48.      Bergstrom J, Hultman E. A study of glycogen metabolism in man. J Clin Lab Invest 1967;19:218–29.[Medline]

49.      Christensen EH, Hansen O. Zur Methodik der respiratorischen Quotient-Bestimmungen in Ruhe and bei Arbeit. Skand Arch Physiol 1939;81:137–71 (in German).

50.      Sondike SB, Copperman N, Jacobson MS. Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents. J Pediatr 2003;142:253–8.[Medline]

51.      Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med 2003;348:2082–90.[Abstract/Free Full Text]

52.      Samaha FF, Iqbal N, Seshadri P, et al. A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med 2003;348:2074–81.[Abstract/Free Full Text]

53.      Stern L, Iqbal N, Seshadri P, et al. The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial. Ann Intern Med 2004;140:778–85.[Abstract/Free Full Text]

54.      Brehm BJ, Seeley RJ, Daniels SR, D'Alessio DA. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J Clin Endocrinol Metab 2003;88:1617–23.[Abstract/Free Full Text]

55.      Yancy WS Jr, Olsen MK, Guyton JR, Bakst RP, Westman EC. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Ann Intern Med 2004;140:769–77.[Abstract/Free Full Text]

56.      Seshadri P, Iqbal N, Stern L, et al. A randomized study comparing the effects of a low-carbohydrate diet and a conventional diet on lipoprotein subfractions and C-reactive protein levels in patients with severe obesity. Am J Med 2004;117:398–405.[Medline]

57.      Westman EC, Yancy WS Jr, Olsen MK, Dudley T, Guyton JR. Effect of a low-carbohydrate, ketogenic diet program compared to a low-fat diet on fasting lipoprotein subclasses. Int J Cardiol 2006;110:212–6.[Medline]

58.      Dansinger ML, Gleason JA, Griffith JL, Selker HP, Schaefer EJ. Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial. JAMA 2005;293:43–53.[Abstract/Free Full Text]

59.      Truby H, Baic S, deLooy A, et al. Randomised controlled trial of four commercial weight loss programmes in the UK: initial findings from the BBC "diet trials. " BMJ Online 2006;332:1309–14.[Medline]

60.      Wood RJ, Volek JS, Liu Y, Shachter NS, Contois JH, Fernandez ML. Carbohydrate restriction alters lipoprotein metabolism by modifying VLDL, LDL, and HDL subfraction distribution and size in overweight men. J Nutr 2006;136:384–9.[Abstract/Free Full Text]

61.      Sharman MJ, Volek JS. Weight loss leads to reductions in inflammatory biomarkers after a very low-carbohydrate and low-fat diet in overweight men. Clin Sci (London) 2004;107:365–9.

62.      Sharman MJ, Kraemer WJ, Love DM, et al. A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men. J Nutr 2002;132:1879–85.[Abstract/Free Full Text]

63.      Dashti HM, Bo-Abbas YY, Asfar SK, et al. Ketogenic diet modifies the risk factors of heart disease in obese patients. Nutrition 2003;19:901–2.[Medline]

64.      Dashti HM, Mathew TC, Hussein T, et al. Long-term effects of a ketogenic diet in obese patients. Exp Clin Cardiol 2004;9:200–5.

65.      Alnasir FA, Fateha BE. Low carbohydrate diet. Its effects on selected body parameters of obese patients. Saudi Med J 2003;24:949–52.

66.      Gann D. A low-carbohydrate diet in overweight patients undergoing stable statin therapy raises high-density lipoprotein and lowers triglycerides substantially. Clin Cardiol 2004;27:563–4.[Medline]

67.      Hickey JT, Hickey L, Yancy WS Jr, Hepburn J, Westman EC. Clinical use of a carbohydrate-restricted diet to treat the dyslipidemia of the metabolic syndrome. Metabol Syndr Relat Disord 2003;1:227–32.

68.      Vernon MC, Mavropoulos J, Transue M, Yancy WS Jr, Westman EC. Clinical experience of a carbohydrate-restricted diet: effect on diabetes mellitus. Metabol Syndr Relat Disord 2003;1:233–7.

69.      O'Neill DF, Westman EC, Bernstein RK. The effects of a low-carbohydrate regimen on glycemic control and serum lipids in diabetes mellitus. Metabol Syndr Relat Disord 2003;1:291–8.

70.      Yancy WS Jr, Vernon MC, Westman EC. A pilot trial of a low-carbohydrate, ketogenic diet in patients with Type 2 Diabetes. Metabol Syndr Relat Disord 2003;1:239–43.

71.      Nielsen JV, Jonsson E, Nilsson AK. Lasting improvement of hyperglycaemia and body weight: low-carbohydrate diet in type 2 diabetes—a brief report. Ups J Med Sci 2005;110:69–73.[Medline]

72.      Nielsen JV, Jonsson E, Ivarsson A. A low carbohydrate diet in Type 1 Diabetes: clinical experience—a brief report. Upsala J Med Sci 2005;110:267–73.[Medline]

73.      Miyashita Y, Koide N, Ohtsuka M, et al. Beneficial effect of low carbohydrate in low calorie diets on visceral fat reduction in type 2 diabetic patients with obesity. Diabetes Res Clin Pract 2004;65:235–41.[Medline]

74.      Hays JH, Gorman RT, Shakir KM. Results of use of metformin and replacement of starch with saturated fat in diets of patients with type 2 diabetes. Endocr Pract 2002;8:177–83.[Medline]

75.      Bailes Jr JR, Strow MT, Werthammer J, McGinnis RA, Elitsur Y. Effect of low-carbohydrate, unlimited calorie diet on the treatment of childhood obesity: a prospective controlled study. Metabol Syndr Relat Disord 2003;1:221–5.

76.      O'Dea K. Westernization, insulin resistance and diabetes in Australian Aborigines. Med J Austr 1991;155:258–64.

77.      O'Dea K. Marked improvement in carbohydrate and lipid metabolism in diabetic Australian Aborigines after temporary reversion to traditional lifestyle. Diabetes 1984;33:596–603.[Abstract]

78.      Robinson E, Gebre Y, Pickering J, Petawabano B, Superville B, Lavallee C. Effect of bush living on aboriginal Canadians of the eastern James Bay Region with non-insulin-dependent diabetes mellitus. Chron Dis Canada 1995;16:1–7.

79.      Volek JS, Feinman RD. Carbohydrate restriction improves the features of metabolic syndrome. Metabolic syndrome may be defined by the response to carbohydrate restriction. Nutr Metab 2005;2:31.

81.      Kossoff EH, Krauss GL, McGrogan JR, Freeman JM. Efficacy of the Atkins diet as therapy for intractable epilepsy. Neurology 2003;61:1789–91.[Abstract/Free Full Text]
82.      Husain AM, Yancy WS Jr, Carwile ST, Miller PP, Westman EC. Diet therapy for narcolepsy. Neurology 2004;62:2300–2.[Abstract/Free Full Text]
83.      Yancy WS Jr, Provenzale D, Westman EC. Improvement of gastroesophageal reflux disease after initiation of a low-carbohydrate diet: five brief case reports. Altern Ther Health Med 2001;7:120, 116–9.[Medline]
84.      Austin GL, Thiny MT, Westman EC, Yancy WS Jr, Shaheen NJ. A very low carbohydrate diet improves gastroesophageal reflux and its symptoms: a pilot study. Dig Dis Sci 2006;51:1307–2.[Medline]
85.      Sladden MJ, Johnston GA. Complete resolution of dermatitis herpetiformis with the Atkins Diet. Br J Dermatol 2006;154:565–6.[Medline]
86.      O'Brien KD, Brehm BJ, Seeley RJ, et al. Diet-induced weight loss is associated with decreases in plasma serum amyloid a and C-reactive protein independent of dietary macronutrient composition in obese subjects. J Clin Endocrinol Metab 2005;90:2244–9.[Abstract/Free Full Text]
87.      van Heel DA, Dart J, Nichols S, Jewell DP, Playford RJ. Novel presentation of coeliac disease after following the Atkins low carbohydrate diet. Gut 2005;54:1342–50.[Free Full Text]
88.      Veech RL. The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism. Prostaglandins Leukot Essent Fatty Acids 2004;70:309–19.[Medline]
89.      Seyfried TN, Mukherjee P. Targeting energy metabolism in brain cancer: review and hypothesis. Nutr Metab 2005;2:30.
90.      Carter JD, Vasey FB, Valeriano J. The effect of a low-carbohydrate diet on bone turnover. Osteoporos Int 2006;17:1398–403 (Epub 2006 May 23).[Medline]
91.      Buse GJ, Riley KD, Dress CM, Neumaster TD. Patient with gemfibrozil-controlled hypertriglyceridemia that developed acute pancreatitis after starting ketogenic diet. Curr Surg 2004;61:224–6.[Medline]
92.      Junig JT, Lehrmann JA. A psychotic episode associated with the Atkins Diet in a patient with bipolar disorder. Bipolar Disord 2005;7:305–6.[Medline]
93.      Beatty SJ, Mehta BH, Rodis JL. Decreased warfarin effect after initiation of high-protein, low-carbohydrate diets. Ann Pharmacother 2005;39:744–7.[Abstract/Free Full Text]
94.      Kalvass JC, Phinney SD, Vernon MC, Rosedale R, Westman EC. Comment: decreased warfarin effect after initiation of high-protein, low-carbohydrate diets. Ann Pharmacother 2005;39:1371–2.[Free Full Text]