Thursday, July 12, 2018

Review: "Fitness Confidential" by Vinnie Tortorich

tl;dr: Recommended, fun and useful account of a top trainer. 
(The links on this page help support the blog!)

For those of us who participate in the health and fitness worlds in podcasts or twitter, Vinnie Tortorich has been a fixture for many years.

Vinnie is "Hollywood's go-to guy for celebrities and athletes looking to get fit fast." He's a "trainer", the guy you go to to lose some pounds and tone up before your next movie role, or for the rest of us, before summer arrives.

Formerly known as "America's Angriest Trainer", (he doesn't really push that line anymore) Vinnie seems to have mellowed in recent years, but you'll still get some of his attitude in this book, originally published in 2013. (You can see him in the photo on the cover, although it's unclear if he's angry about the dietary idiocy foisted on Americans, angry about a client not listening, or just in agony while on an ultra-length bicycle ride.)

What you get in this book is Vinnie's biography, essentially, peppered with mostly anonymous stories of his experiences in his own life that shaped his approach to training people. Despite the subtitled tease "get the dirt", one of the things you won't find in this book is dirt on clients. Vinnie doesn't kiss and tell and name names, although there are a few names mentioned. Interestingly, one of the non-anonymous clients Vinnie discusses is his co-author, Dean Lorey, who fired Vinnie initially after finding his approach challenging.

Lorey came around, wound up thin and running a half-marathon, and then proceeded to nag and coach a reluctant Vinnie into writing this book together.

The result is a well-written and quick read. You won't find pages of recipes or workout routines, instead you'll find concise principles that (in my experience, independent of Vinnie) will work, and lots of entertaining stories to illustrate the principles and drive them home.

Of more value is Vinnie's advice on how to select a gym, and trainer, some real useful thoughts about what works and what doesn't, and tips on how to help people get motivated. Some of it is quite counter-intuitive.

I read this book on a flight from LA to NYC, and it kept pulling me along.

The surprising thing about this book, perhaps, is that he's not an angry guy, he's caring and thoughtful, and seems to be motivated to continue his career by a genuine desire to help people, both his clients and the rest of us.

N.B. When you reach the advertised "end" of the book, keep reading. The best part, I thought, was in the chapters after the story of the training and diet stuff is over. This is the story of Vinnie's battle with leukemia and his fight to conquer a 509.5-mile bicycle race through Death Valley. It's the best part of the book, in my opinion, and is not to be missed.

Overall, it's highly recommended. If you're looking for a simple and straightforward recipe for weight loss and fitness, this is a fun and entertaining way to get it, and you'll wind up with a better approach than most PhDs.

FITNESS CONFIDENTIAL: Adventures in the Weight-Loss Game

Wednesday, July 4, 2018

"Why the carbohydrate-insulin model of obesity is probably wrong: A supplementary reply to Ebbeling and Ludwig’s JAMA article"


Link via Stephan J. Guyenet, PhD

Thursday, June 28, 2018

What's Worse—Carbs or Seed Oils? Understanding a High-PUFA Diet.

tl;dr: The one study I'm aware of that shows conclusively that excess glucose acts as an accelerant for excess n-6, but it not nearly so harmful without the n-6, in vivo.

I had this study:

As my pinned tweet on Twitter for quite a while. (N-6 is short for omega-6 fats). The argument has gotten a little stronger since then, but the study is important to understand, as it best elucidates the mechanism behind the argument concentrated omega-6 fats and not carbohydrates alone are the best candidate for the root cause of the Diseases of Civilization.

This is the one study I'm aware of that shows conclusively that excess glucose acts as an accelerant for excess n-6, but it not nearly so harmful without the n-6, in vivo.

"Brief episode of STZ-induced hyperglycemia produces cardiac abnormalities in rats fed a diet rich in n-6 PUFA" (PDF) [1]

A title only an editor could love, as it buries the lead deeply enough so it could only be found by an archaeologist.

What are they trying to show here?
"Diabetic patients are particularly susceptible to cardiomyopathy independent of vascular disease, and recent evidence implicates cell death as a contributing factor. Given its protective role against apoptosis, we hypothesized that dietary n-6 polyunsaturated fatty acid (PUFA) may well decrease the incidence of this mode of cardiac cell death after diabetes." 
"...The majority of studies that have looked at the relations between lipotoxicity and cardiovascular complications of diabetes have utilized lard or other sources of saturated dietary fat rich in palmitic acid (7, 17, 26). However, in humans, increased awareness of obesity and its cardiovascular complications have led to an indiscriminate substitution of atherogenic saturated cooking fats with “heart-friendly” refined vegetable oils, such as sunflower oil, rich in n-6 polyunsaturated fatty acids (PUFA) (42). In several studies, n-6 PUFA conferred protection against arrhythmias (32) and coronary artery disease (12) and, at least in human primary fibroblasts and Leydig cells, prevented apoptosis (4, 31)."
Excellent, seed oils (a more precise term than vegetable oils) are the primary source of such fats, and they're what the Dietary Guidelines suggest we eat to stave off heart disease.

Cardiomyopathy is, basically, a failure of the muscles in the heart. They don't entirely fail, but it's progressive, and also leads to heart failure, which also doesn't indicate total failure, but is obviously not good.

It's not good, but it's also common, and one can find many articles with titles like:

"Heart failure: the cardiovascular epidemic of the 21st century" [2]

Or more alarmingly:

"Impact of Obesity and the Obesity Paradox on Prevalence and Prognosis in Heart Failure" [3]

Prevalence of heart failure in 5,881 Framingham participants according to obesity status.
So avoiding cardiomyopathy and heart failure is a hot topic.

So what, again, are they doing?
"We hypothesized that, given the role of saturated fatty acids in accelerating cardiac apoptosis after diabetes, switching to an n-6 PUFA-rich diet may well be protective against cell death."
They're trying to test what happens with the "indiscriminate" replacement of saturated animal fats with seed oils in diabetics, using a mouse model.

Since they have a control that is fed a high-carbohydrate diet, both with and without induced diabetes, this also serves as a comparison of the effects of carbohydrates and n-6 PUFA on these animals, although this was not the focus of the paper. As the effects are fairly dramatic, I will highlight those parts.

So here are the steps:
  1. Table 1. Composition of diets
    Determine diets. They picked two, and added sunflower to one as a PUFA source. Diet details are good, pretty well-controlled by the generally-abysmal standards of these studies, but they aren't perfectly matched diets like in this study. One has a fair bit more carbs, and the PUFA diet has 2X the monounsaturated fat, 9X the n-6 PUFA, and 1/3 the n-3. Saturated fat was about the same. (See table 1.)
  2. Table 2. About the recently-deceased rats
    Acquire rats, divide into 4 groups, divided by the traits: Diabetic (D), and Normal (N), and Control (C), and PUFA (P). This gives us Normal Control (NC) Normal Diabetic (ND), and PUFA Control (PC) and PUFA Diabetic (PD) rats. (See table 2.)
  3. Feed all the rats their diets for 4 weeks.
  4. Give the rats in ND and PD groups T1 diabetes by injecting enough STZ (streptozotocin) to kill half the beta cells in the pancreas.
  5. Let the now type 1 diabetic D-group rats eat for 4 days.
  6. Take serum blood samples, then kill all the rats for analysis.
The Good News
"...We hypothesized that dietary n-6 polyunsaturated fatty acid (PUFA) may well decrease the incidence of this mode of cardiac cell death after diabetes." 
Apoptosis is a process of controlled cell death, which allows the body to get rid of damaged cells before say, they become cancerous. While many in the online community get worked up about it, and pursue it through fasting, it's really just a basic house-keeping process, that probably goes on all the time. It's certainly plausible that too much apoptosis could be a bad thing, just as too much of anything could be bad. Clearly having too many heart cells (myocytes) die off could be problematic, and would explain much of heart failure.
"Recently, we demonstrated that feeding a 20% (wt/wt) palm oil diet (rich in palmitic acid) to diabetic rats enhances cardiac apoptosis in vivo..."
Fig. 2. Apoptosis protection from n-6 PUFA
They tracked "....caspase-3 activity, the prime effector of cardiomyocyte apoptosis..." and sure enough, apoptosis in the PUFA-fed diabetic rats (PD) was much lower than the non-PUFA fed diabetic rats (ND).  Apoptosis in PD was a bit higher than NC or PC, but as a treatment this appeared to be a very good thing. See the red-highlighted bars in Fig. 2 to compare ND to PD. N-6 PUFA for the win!

However, they also checked heart function by another method. They looked at necrosis, and at the heart muscle directly:
"To verify necrosis, serum LDH [lactate dehydrogenase] was estimated using an appropriate kit (Sigma). However, release of LDH does not necessarily imply cardiac necrosis. Thus, to verify cardiac necrosis, sections were evaluated histologically using Masson’s trichrome stain..."
The Bad News

Fig. 3. Necrosis via lactate dehydrogenase
Necrosis is a catastrophic cell death (they use the word "accidental", but it's a bit worse than that) that leads to uncontrolled release of cell contents into the body. Some of these are toxic, and some can induce auto-immune responses, which is why the body prefers to use the orderly process of apoptosis.

In Fig. 3 we can see that LDH skyrockets in the PD rats , those that showed a major benefit from n-6 "control" of apoptosis. It appears that what n-6 is actually doing is shifting the cells from controlled, apoptotic cell death to uncontrolled, necrotic cell death.
"In these hearts, a rise in linoleic acid and depleted cardiac glutathione could explain this “switch” to necrotic cell death."
But they did mention that it's not a sure-fire indicator, and so they had a visual check of heart cells as a backup method.

Fig. 3 A. Normal heart (NC) Fig. 3 D. Necrotic heart (PD)
"Black arrows, severe disruption of contractile apparatus (hypercontracted muscle and thickened fibers); white arrows, focal necrosis (gray discoloration) in... PD hearts (D, 600). Cardiac necrosis was absent in NC (A, 400)..."
Indeed it appears that the n-6 + diabetes rats have suffered a catastrophic onset of heart failure via necrosis. In just four days! N-6 did indeed "protect" them from apoptosis, by shifting to a worse outcome.

More Bad News: Cardiolipin Levels Collapsed, as Did Mitochondria

I've written three long posts on the role and impact of excess n-6 in the mitochondria as affects cardiolipin (CL):
  1. The Cause of Metabolic Syndrome: Excess Omega-6 Fats (Linoleic Acid) in Your Mitochondria
  2. How To Prevent Oxidative Damage In Your Mitochondria
  3. What Effect Does Linoleic Acid Have On Mitochondria?
So I won't bore you here. To summarize, CL is a key molecule in the mitochondria that preferentially takes up n-6, and then breaks down into toxins such as HNE, often destroying the mitochondria, and perhaps the cell, in the process.

Here we have an n-6 intervention, with resultant cell death via necrosis. Was CL in the mitochondria involved, as my posts above would predict?

Fig. 5. Cardiolipin
Luckily these researchers looked at it.

Figure 5 shows the catastrophic effect of n-6 on cardiolipin in both wings to which it is fed, and the much smaller, but still additive, effect of induced diabetes.
"Total cardiolipin decreased almost sixfold after n-6 PUFA feeding, with a significant drop of ATP only in PD hearts, which could have contributed to cardiac necrosis (40)." 
As CL is a crucial molecule in the mitochondria, one would expect that such a dramatic reduction in CL content would also have an effect on the mitochondria, since CL is required for ATP production. (ATP is the body's basic energy carrier.) The paper also looks at morphology, the shape of the mitochondria, both normal and n-6-fed.
"Figure 5A depicts a mitochondrion with a double membrane and lamellar cristae, which are typical in NC, ND, and PC hearts. A novel observation in this study was abnormal condensed mitochondria, but only in the PD group (Fig. 5B)." [Image A not shown]
Fig. 5 B. Normal mitochondria (orange), condensed (red)
Hence n-6 consumption has a catastrophic effect on mitochondria, and hyperglycemia induces even worse pathology.

Bad News Continues: Mitochondrial Function Reduced

The next question is the functional impact of these alterations of CL content and mitochondrial form.

The authors therefore look at the effect of these alterations on fuel use.

Fig. 6 B. Glucose (white) and palmitate (black) use
And sure enough, they were rather severe. The authors (details in the paper) take the hearts from the dead animals and run fuel through them, creating a controlled environment where they can see precisely what fuel is used and how much.
"To meet the energy demand at high afterload (135 mmHg), all except the PD group increased their glucose oxidation. With regard to fatty acid oxidation, only the NC group was able to increase palmitate oxidation, suggesting that, in the ND, PC, and PD groups, fatty acid oxidation was already operating at its maximum at low afterloads."
The lack of glucose oxidation (red circle, Fig. 6 B) indicates a near-total failure in mitochondrial Complex I, where glucose is burned. The study detailed in my post 3 notes a high production of reactive oxygen species (ROS) in complex I induced by n-6, and the results of this study suggest that n-6 induced ROS may terminally damage complex I and thus the cell's ability to utilize glucose.
"A novel observation in this study was that, analogous to Barth’s syndrome, n-6 PUFA feeding for 4 wk, together with 4 days of hyperglycemia, led to similar changes in some mitochondria. Interestingly, abnormal condensed mitochondria have been recently recognized in skeletal muscle and cardiac atrial neurons from diabetic patients (25)."
This is a notable finding, as excess ROS production and an inability to utilize glucose is a primary feature of Alzheimer's Disease, which is also referred to as Type III Diabetes and for  which n-6-induced damage is an oft-observed possible cause.

Mitochondrial Toxins Increased

Fig. 4 A GSH in Control (white), Diabetic (black)
In my post 2 above I noted that the breakdown of n-6 fat linoleic acid in CL produces a toxin, HNE. As production of some amount of HNE is a normal part of mitochondrial function, there's a detoxification mechanism, part of which is the antioxidant glutathione—inexplicably abbreviated everywhere as GSH. While the authors don't mention HNE directly—the mechanism for CL producing HNE wasn't found until 2012—they do look at GSH. Since GSH levels are often used as a proxy for HNE production, this is a useful measure.
"PUFA feeding was associated with a significant decrease in GSH. Interestingly, diabetes for 4 days in normal chow-fed rat hearts could not decrease cardiac GSH, whereas superimposition of diabetes in PUFA-fed animals led to a further decrease in cardiac GSH levels (Fig. 4A)"
In Fig. 4 A, one sees that GSH is indeed reduced, least in ND rats, most in PD rats. There is additional discussion in the paper about some further indicators, but I'm not going to discuss them as they don't add much to the point made here. 

HNE is the leading cause of genetic damage and also induces amyloid-beta plaque development in Alzheimer's, so it's something we want to minimize, and the implication of this data is that n-6 in these amounts overwhelms the body's ability to detoxify it.

This would explain one of the more inexplicable aspects of chronic diseases of civilization, that of mitochondrial dysfunction. Here it is shown how to induce it.

Worst News: Now They Have Heart Failure

The failure in energy production, as the mitochondria are the primary engines of the heart, has consequential effects on heart function. Function decreases, and the ability to respond to increased demands declines dramatically, as the semi-functional mitochondria are no longer able to meet those demands.
Fig. 8. Heart function
"At higher afterloads, glucose and fatty acid oxidation increased in the NC group. In ND and PC hearts, the only increase was that of glucose oxidation, inasmuch as, presumably, fatty acid oxidation was already operating at its maximum. The PD group alone failed to increase its glucose oxidation in response to a higher energy demand, an aspect that could have contributed to the drop in cardiac function."
Additionally, they have some spiffy pictures of the progression of cellular dysfunction from NC to the poor PD rats, who are clearly in a rough spot. I'll spare you those, as I presume by now the gist is clear.

This failure of the capacity to produce energy using fats causes a back-up of fats in the fat cells, as delivery is exceeding demand.
"In our study, n-6 PUFA feeding substantially increased cardiac fatty acid in the PC and PD groups, but only PD hearts demonstrated a considerable increase in lipid droplets."
They've replicated what's described in this paper [4], in the section entitled "Evidence that Human Cardiac Dysfunction Is Associated with Excess Lipid", where lipid droplets are seen in diabetic and/or failing human hearts.

N-6 Induced Obesity

The weight figures from Table 2 fail to tell an important story. The figures given are those when the rats were killed, but the highest weight in the D-groups was at STZ injection. See the chart (mine) to see what a significant increase n-6 caused in the rats' weights prior to STZ, which caused a dramatic decline only in the rats fed n-6.

Rat weight at STZ injection.
Red indicates weight lost after injection (4 days)
"Interestingly, in contrast to the ND group (361 ± 9 and 358 ± 9 g before and after STZ, respectively), diabetes in PUFA-fed animals was associated with a profound loss of body weight (450 ± 11 and 393 ± 11 g before and after STZ, respectively). This loss in body weight could not be attributed to any change in food or fluid intake but could be a result of excessive lipolysis and loss of adipose tissue mass with subsequent increases in serum free fatty acids and TG in the PD group."
This is consistent with Alvheim's series of papers starting in 2012 showing that n-6 linoleic acid uniquely induces obesity in rodents. [5]

A Bonus Bad-News Easter Egg: The Control Got Diabetes, Too 

"Thus, although promoted as being beneficial, excess n-6 PUFA, with its predisposition to induce obesity, insulin resistance, and ultimately diabetes, could accelerate myocardial abnormalities in diabetic patients... Circulating TG were higher in the PC than in the NC group, and serum insulin was increased in the PC group (likely as a consequence of insulin resistance) compared with the NC group, but there was no overt hyperglycemia in the PC group."
Table 2. PC is PUFA Control, not the intervention!
They don't really focus on this, but it's kind of a big deal. They had two variables they were testing, and this left them with four groups, as detailed in Table 2. Therefore they had one "control", NC, but the intervention was supposed to be the PD group. But let's look at the PC group, too. The quote above notes they didn't get "overt" hyperglycemia, but, compared to the full control, their:
  • Blood glucose +29%
  • Triglycerides (TG) +462%
  • Insulin +96%
  • Leptin* +59%
(* An hormone that is supposed to control fat accumulation.)

The D-groups had Type 1 diabetes induced, the PC group got Type 2 diabetes because of the intervention: n-6 induced it!

Back to "overt" hyperglycemia. The PC rats didn't get it because:
"In rodents fed high-fat diets, insulin resistance does not progress to hyperglycemia in the absence of genetic defects (36)."
So these rats seem to have gotten as close to Type 2 diabetes as it's possible for them to have gotten.

"In summary, chronic caloric excess of n-6 PUFA when coupled with acute diabetes of only 4 days precipitated mitochondrial abnormalities, a steep drop in GSH, altered substrate utilization, and myocardial TG deposition. Given that these hearts also demonstrated necrosis and extensive myocardial cell loss, a feature that is predominant only in chronic diabetes (1, 14, 16, 24), our data suggest that this mode of cell death in PUFA-fed diabetic hearts is an important factor in accelerating diabetic cardiomyopathy. Although these effects of n-6 PUFA in the diabetic animal would seem contrary to accepted belief as being beneficial, in countries such as Israel, with high dietary n-6 PUFA consumption, there is an excessive incidence of obesity, insulin resistance, hypertension, and type 2 diabetes (6).... Thus advocating diets rich in n-6 PUFA for diabetic patients could accelerate the impairment of myocardial contractility."
This also is the only study I know of that shows the effects of hyperglycemia to significantly accelerate the negative effects of n-6 PUFA feeding on an organism. The PC and PD groups can be seen as a model for the progression of obesity and insulin/leptin resistance to an advanced form of chronic Type 2 with advanced pancreatic beta-cell death, a condition that is becoming increasingly common in human children.

Combined with my previous post, "Hello, Can We Have Your Liver?": Understanding a High-PUFA Diet, we have evidence of n-6 involvement in two major chronic organ failures, and the hints of causation of diabetes, a disease impacting all organs.

(I'll also note that I've been told this paper was a Trojan horse, that the authors knew very well what the paper was going to show, but to get it published kow-towed to the Temple of Vegetable Oils, to make it look like another cheerleading pro-PUFA study. They feign surprise that this does not seem to be the case, but I think that in this sentence, with it's pejorative "indiscriminate" and scare quotes around "heart-friendly", they let the truth slip out. Luckily the editors and reviewers didn't catch it!
"However, in humans, increased awareness of obesity and its cardiovascular complications have led to an indiscriminate substitution of atherogenic saturated cooking fats with “heart-friendly” refined vegetable oils, such as sunflower oil, rich in n-6 polyunsaturated fatty acids (PUFA) (42)."
Good for them!)

[1] Ghosh, Sanjoy, Dake Qi, Ding An, Thomas Pulinilkunnil, Ashraf Abrahani, Kuo-Hsing Kuo, Richard B. Wambolt, Michael Allard, Sheila M. Innis, and Brian Rodrigues. Brief episode of STZ-induced hyperglycemia produces cardiac abnormalities in rats fed a diet rich in n-6 PUFAAm J Physiol Heart Circ Physiol 287: H2518 –H2527, 2004. First published July 29, 2004; doi:10.1152/ ajpheart.00480.2004

[2] Thomas F. Lüscher. Heart failure: the cardiovascular epidemic of the 21st century, European Heart Journal, Volume 36, Issue 7, 14 February 2015, Pages 395–397,
[3] Carl J. Lavie, Martin A. Alpert, Ross Arena, Mandeep R. Mehra, Richard V.Milani, Hector O. Ventura. Impact of Obesity and the Obesity Paradox on Prevalence and Prognosis in Heart Failure
JACC: Heart Failure Apr 2013, 1 (2) 93-102; DOI:10.1016/j.jchf.2013.01.006

[4] Goldberg, Ira J. et al. Lipid Metabolism and Toxicity in the Heart, Cell Metabolism, Volume 15 , Issue 6 , 805 - 812

[5] Alvheim, A. R., Malde, M. K., Osei‐Hyiaman, D. , Hong, Y. H., Pawlosky, R. J., Madsen, L. , Kristiansen, K. , Frøyland, L. and Hibbeln, J. R. (2012), Dietary Linoleic Acid Elevates Endogenous 2‐AG and Anandamide and Induces Obesity. Obesity, 20: 1984-1994. doi:10.1038/oby.2012.38

Wednesday, June 6, 2018

Thoughts on "Cardiolipin Synthesis in Brown and Beige Fat Mitochondria Is Essential for Systemic Energy Homeostasis"

Interesting confirmation of a core mitochondrial functional role for cardiolipin, and some interesting observations about cold-adaptation.

Get used to shivering! 
"However, the ability of adipose tissue to expend energy is a dynamic process that continues to increase with prolonged cold exposure, only reaching maximal capacity after several weeks (Cannon and Nedergaard, 2004)."
And clearly staying warm is overwhelmingly dependent on fat metabolism.
"However, the enrichment of lipid metabolism proteins far eclipsed that of proteins involved in all other metabolite pathways from 3 days to 3 weeks of cold exposure (Figure 1B)."
This likely explains why overweight people or inactive people have such a problem staying warm. Fat-burning capacity is dependent on stimulus, and while this doesn't show it, it likely atrophies like every other function of the body. Use it or lose it.

One of the key questions around cardiolipin and omega-6 fat intake is: what is a cardiolipin supposed to look like? This is more evidence that they're not supposed to be saturated with linoleic acid, leaving them uniquely susceptible to oxidizing and producing toxins like HNE as they damage mitocondrial function.
"Newly synthesized CL is characterized by shorter, more saturated acyl chains, which can be remodeled by phospholipases, and acyltransferases through monolysocardiolipin (monolysoCL) intermediates to generate a diverse pool of CLs."
It shouldn't surprise that CL is produced in an ideal state. Why it so readily takes up linoleic acid is an interesting question...

The paper also claims that energy production in brown-fat adipocytes (fat cells) controls systemic glucose homeostasis and therefore type 2 diabetes.

I'm a little more skeptical of that claim, as I looked into the connection between mitochondrial dysfunction and diabetes, and it's not as clear as I would like it to be. If this was a clear mechanism, then it would suggest that people living in warm climates that never experience a need for cold thermogenesis would be more susceptible to diabetes, and we really don't see that.

They get it when the industrial diet is introduced, same as everyone else on the planet.

Friday, April 27, 2018

LDL Cholesterol: You Aren't Always What You Eat, or Roundabout Ways to Improve Your Diet

Sometimes you read these papers and shake your head.

"Lowering Dietary Saturated Fat and Total Fat Reduces the Oxidative Susceptibility of LDL in Healthy Men and Women"

The troll who pointed me to this was trying to argue that this invalidated the claim that omega-6 polyunsaturated (n-6) fats are important in cardiovascular disease (I gather), since lowering saturated fat (see the title) lowered oxidation.

Oddly enough, he was almost right, but not quite.

Fat components
The intervention was to have fixed protein (15%), but a variable rate of saturated fat (SFA), to be replaced by carbohydrate (CHO), and fixed rates of monounsaturated and polyunsaturated fats (MUFA and PUFA, respectively). And they did a good job of detailing what the diet included, right down to the individual fats.

However you have to go to a different study to find all the details ("Effects of Reducing Dietary Saturated Fatty Acids on Plasma Lipids and Lipoproteins in Healthy Subjects")

To sum the variation, SFAs were 16%, 9%, and 5%; and CHO was therefore 48%, 55%, and 59%. MUFA was 14%, and PUFA was 7%.

The diet part of it seems to have been very well done, indeed. If you want some idea from where the food may have come, may I introduce you to their sponsors?
"The DELTA Investigators express thanks to the following contributors: AARHUS, Bertolli, USA., Best Foods, Campbell Soup Company, Del Monte Foods, General Mills, Hershey Foods Corp., Institute of Edible Oils and Shortenings, Kraft General Foods, Land O'Lakes, McCormick Incorporated, Nabisco Foods Group, Neomonde Baking Company, Palm Oil Research Institute, Park Corporation, Procter & Gamble, Quaker Oats, Ross Products Division/Abbott Laboratories, Swift-Armour and Eckrick, Van Den Bergh Foods, Cholestech, Lifelines Technology Incorporated."

The troll was almost right because LDL oxidation did indeed go down in this study. But it went down for a reason that I wouldn't have expected, and which leaves me somewhat perplexed to explain mechanistically. 

The paper goes on ad nauseum along these lines:
"Convincing evidence suggests that oxidative modification of LDL plays an important role in the pathophysiology of atherogenesis (Steinberg 1997). In recent years, numerous molecular mechanisms have been proposed to explain the different oxidation pathways that lead to modification of LDL (Steinberg 1997). 
"One of the earliest steps in the generation of oxidatively modified LDL is the peroxidation of its polyunsaturated fatty acids (PUFA).3 The oxidative breakdown products of these fatty acids, such as malondialdehyde [MDA] and 4-hydroxynonenal [HNE], form covalent bonds with apolipoprotein B (apo B)..."
Yeah, yeah. Old news (the paper is from 2000), but here's where it gets odd:
"The results of the present study also show that LDL composition (LDL quality) affects susceptibility to oxidation. [It] was inversely correlated with the quantity of LDL oleic acid (r = −0.29, P < 0.01), and positively correlated with the quantity of LDL linoleic acid (r = 0.23, P = 0.04) and the 18:2-to-18:1 ratio (r = 0.52, P < 0.001). The oxidation rate was positively correlated with the 18:2-to-18:1 ratio (r = 0.24, P = 0.03)."
To lower n-6, cut SFA?


So lowering SFA indeed made the LDL more resistant to oxidation. But it did so by lowering n-6 and raising MUFA in the LDL! SFA was basically unchanged.

A little Lipidology 101, MDA and HNE, mentioned above, aren't made from SFA, they're made from PUFA, and HNE is made exclusively from n-6. MDA and HNE pretty much are oxidized LDL. So you're not getting oxidized LDL from SFA in the body. It just won't happen.

Of course the authors don't mention that little fact. More below.

For some reason I am unable to explain, lowering SFA (16:0, palmitate in the chart) in the diet lowered n-6 (18:2, linoleate) in the LDL, and increased MUFA (18:2, oleate), protecting LDL from oxidation. SFA stayed  the same, basically.

My best guess is that it was the increased CHO in the diet (is this what's behind the Japanese diet, which is low in SFA and high in CHO?) but it is just a guess.
"In the present study, the ratios of 18:2 to 18:1 and PUFA to MUFA in the LDL from subjects when they consumed the Step-1 and Low-Sat diets were significantly lower than they were in the LDL from subjects when they consumed the AAD. Linoleic acid (n-6) in LDL from subjects when they consumed the Low-Sat diet also was significantly lower compared with those from subjects when they consumed the AAD. "
The first citation for this paper is:

"Oxidation of low-density lipoproteins: intraindividual variability and the effect of dietary linoleate supplementation"
"LDL oxidized faster after the linoleate diet than after the oleate diet... and produced more conjugated diene [that's bad] in proportion to the increase in LDL linoleate."
Here's where we get to the shaking my head part.

Why in blazes wouldn't you reduce the thing that is actually capable of causing the harm, as your first cite shows, and as your own study shows, is the source of the problem? Why keep n-6 flat and reduce something else, which through some round-about effect, lowers what you need to lower, the n-6?

Just lower the n-6 and you reduce the susceptibility for oxidation! They cite other papers that have done exactly that!

This study was done in 2000, did I mention that?

Think of the progress we would have made if they'd actually done what any engineer reading this paper would have told them to do. 
"N-6 converts to these toxins? You're proved that? Why not reduce the n-6?"
Let's not get too into conspiracies here, but on the face of it this study is clearly little more than a misleading advertisement for the sponsors listed above, who are forced to follow the United States Dietary Guidelines and replace saturated fats with the n-6 fat that their own research claims is harmful.

This post started with a twitter troll who cited the first-mentioned study: