A Sneak Peek at “Carb-Loaded”

Carb-Loaded

Now you can watch a 3-minute trailer for the movie Carb-Loaded. It’s about the low-fat, sweet and floury causes of the obesity epidemic:

A sneak peek at “Carb-Loaded

Note also that there are subtitles in English and a few other languages. To chose a language, click on “CC” in the lower, right corner.

One of the interviews contains an explanation that I think sounds odd – how the body releases cholesterol to repair injuries to arteries. That is a metaphor that I’m not quite buying.

That small injuries to arteries and inflammation are central to heart disease is, however, probably true. As mentioned in the video, the result is like an abrasion on the inside of the arteries, that never heals completely.

Many things may contribute to injuries and resulting inflammation in the arteries, for example high blood sugar, high blood pressure, toxic substances from smoking and rancid small dense LDL cholesterol particles (which is primarily a result of too many bad carbohydrates in your diet).

What do you think about the video?

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21 comments

Top comment

  1. Murray
    I've spent several years now reading on cholesterol and arterial sclerosis. I find it astounding that this has been a pressing issue since at least the heart attacks of President Eisenhower and yet there is still no plausible theory established by science as to the mechanism of what happens.

    I find what might be called the "gradient" theory--that some threshold concentration of bad cholesterol-containing particles causes damage to endothelial walls or magically embed themselves--not to be plausible. There are too many cases where arteries are perfectly clear except for specific areas.

    I find much more plausible the hypothesis that the various insults to the robustness of endothelial lining mentioned make it vulnerable to sheer stress damage at various locations. LDL cholesterol particles are ferried into those spots for repair. I haven't seen any evidence that the damaged locations send signals to the liver to increase cholesterol production. Perhaps so, but I haven't seen that yet.

    It seems the problems arise when too much of the cholesterol containing particles that arrive are compromised. The small dense LDL are the ones most likely to have oxidized cholesterol, which get tagged by Lp(a) for destruction by macrophages, resulting in inflammation and cholesterol-macrophage accumulation at the damage sites. I expect the effective buoyant LDL that are not oxidized get in the site just as much, but do not get tagged by Lp(a) and leave when they have made their delivery. So it is only the small dense LDL that remain at the scene of the crime. Add to this the calcium attracting effect of an increased ratio of sphingomyelin around arterial cells from diet high in omega-6 oils and other oxidized fats (as per Fred Kummerow's findings) and one gets calcified plaque forming at the site of the inflammation. Put this in the context of a diet low in vitamin K-2, D3 or retinol, and calcification is less likely to be removed over time with resolution of the inflammation.

    This plot synopsis doubtless omits some major characters in the play, but it seems much more plausible to me than accounts that suggest the sd-LDL somehow penetrate the endothelial lining like sand or something and cause problems.

    Of course there are huge vested interests in the cholesterol paradigm of cardiovascular disease that I expect research funding into more plausible alternatives is effectively blocked. Pity. I look forward to the day there is an explanation that is actually plausible. What I see now are rationalizations with appeals to magical processes meant to misdirect people away from genuine inquiry.

    Reply: #5
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  1. FrankG
    Here we go again :-P I'm anticipating a wave of comments about how bad this is, or how it could have been done better... just please remember to not let perfection become the enemy of good.

    Maybe the naysyaers should make their own documentary, so we can pick holes in that as well?

    On the cholesterol topic: it does make sense to me that cholesterol is a significant part of the body's repair mechanisms. Isn't it used in every cell wall?

    They touched on the "firefighter" analogy which I ilke... there is an almost 100% correlation between firefighters and house fires (just like atherosclerotic plaques and cholelsterol)... so should we therefore conclude that firefighters cause house fires?

  2. Sue
    'how the body releases cholesterol to repair injuries to arteries. That is a metaphor that I’m not quite buying.'

    This is actually the thing that all the people shown in the clip agree on. If you research any of what they do they explain it beautifully. (I personally found Gary Taubes to be the easiest to understand)

    Basically, cholesterol is the way our bodies heal. I think in the next ten years even the most die hard will have to accept the reality.

    I love that it is coming out now, hopefully not too late to repair the damage I have already done to my body.

  3. Murray
    I've spent several years now reading on cholesterol and arterial sclerosis. I find it astounding that this has been a pressing issue since at least the heart attacks of President Eisenhower and yet there is still no plausible theory established by science as to the mechanism of what happens.

    I find what might be called the "gradient" theory--that some threshold concentration of bad cholesterol-containing particles causes damage to endothelial walls or magically embed themselves--not to be plausible. There are too many cases where arteries are perfectly clear except for specific areas.

    I find much more plausible the hypothesis that the various insults to the robustness of endothelial lining mentioned make it vulnerable to sheer stress damage at various locations. LDL cholesterol particles are ferried into those spots for repair. I haven't seen any evidence that the damaged locations send signals to the liver to increase cholesterol production. Perhaps so, but I haven't seen that yet.

    It seems the problems arise when too much of the cholesterol containing particles that arrive are compromised. The small dense LDL are the ones most likely to have oxidized cholesterol, which get tagged by Lp(a) for destruction by macrophages, resulting in inflammation and cholesterol-macrophage accumulation at the damage sites. I expect the effective buoyant LDL that are not oxidized get in the site just as much, but do not get tagged by Lp(a) and leave when they have made their delivery. So it is only the small dense LDL that remain at the scene of the crime. Add to this the calcium attracting effect of an increased ratio of sphingomyelin around arterial cells from diet high in omega-6 oils and other oxidized fats (as per Fred Kummerow's findings) and one gets calcified plaque forming at the site of the inflammation. Put this in the context of a diet low in vitamin K-2, D3 or retinol, and calcification is less likely to be removed over time with resolution of the inflammation.

    This plot synopsis doubtless omits some major characters in the play, but it seems much more plausible to me than accounts that suggest the sd-LDL somehow penetrate the endothelial lining like sand or something and cause problems.

    Of course there are huge vested interests in the cholesterol paradigm of cardiovascular disease that I expect research funding into more plausible alternatives is effectively blocked. Pity. I look forward to the day there is an explanation that is actually plausible. What I see now are rationalizations with appeals to magical processes meant to misdirect people away from genuine inquiry.

    Reply: #5
  4. Alain
    Dr Peter Attia - The Straight Dope on Cholesterol

    http://www.youtube.com/watch?v=dAWdHYSrh7M

  5. Boundless
    > ... pressing issue since at least the heart attacks of President Eisenhower ...

    It's a tradition in the US for Presidents to be killed by their doctors, going back to George Washington. In Ike's case, it was Paul Dudley White, a lipid hypothesis advocate clone of Ancel Keys.

    > ... research funding into more plausible alternatives
    > is effectively blocked. Pity. I look forward to the day
    > there is an explanation that is actually plausible.

    More likely, the general public is going to figure out on their own how to simply make CVD disappear as a problem, which will then become a purely academic question of "Say, what used to cause heart disease, anyway?"

    Reply: #6
  6. FrankG
    As predicted in 1973 by Woody Allen's film Sleeper..? :-)

    http://www.youtube.com/watch?v=1yCeFmn_e2c

    Reply: #7
  7. Boundless
    > As predicted in 1973 by Woody Allen's film Sleeper ...

    Yep. I've referenced that scene myself on another blog a few years ago.

    It's become kind of cliche for the sloppy science we've fallen victim to. Here's a typical recent link by another blogger:
    http://www.datasciencecentral.com/profiles/blogs/bad-data-science-and...

    However, I suspect that what Woody's intent was more about ribbing his acquaintances for their food fads than in forecasting some weighty future truth about human nutrition.

  8. Lady Dee
    I have inherited high Cholesterol (200-250) and High Blood Pressure (In the 130's/high 80's or 90's). Not on meds yet but every year I have to have a physical for my job and they threaten me with meds. I barely get away with it.
    I feel fine and have recently lost 35 lbs. on LCHF diet. So how am I and hubby going to keep our jobs? We have to go to Dr.'s of companies choice.
    We are going to continue this lifestyle and see what happens by next summer.
    Reply: #10
  9. Sue
    Lady Dee, the change in diet should have a dramatic effect on your blood pressure and cholesterol but it is not a magic bullet.
    What other health issues do you have? Do you sleep well? I just found out I have massive sinus polyps (the reason I did not sleep well) and now am trying to find a doctor who will help me work out exactly what caused these, rather than just throw me on steroids for life.
    Whilst you have to have your check up through the company doctor, you can find a doctor who you feel comfortable with to help you with your health issues.
  10. Lori Miller
    LC typically improves blood pressure.

    If they give you a statin prescription, accept it and throw it away when you get home.

  11. LadyDee
    Sue - I have no health issue, not on any meds. I am new to the LCHF lifestyle so I know it will take awhile. Not to mention I went a little crazy and had carbs and sugar for a few wks. before getting blood work. LOL Now we are back on track! I'm still learning exactly what to do and eat. Hubby did have to go on meds for BP but he is done now and is not taking anymore. Deep breathing for 15 min prior to 2nd check-up helped a lot! His cholesterol has always been great!

    Lori - Sounds good to me!! I'm good for this year.

  12. gotlucky
    I think I'm excited to see the movie!!
  13. Paul the rat
    Good story. Do you think that CICO crowd is as hopeless in other aspects of their lives as they are about CICO? (sorry folks I am unable to post whole paper)

    Econ Hum Biol. 2014 Jul;14:33-49. doi: 10.1016/j.ehb.2014.04.002. Epub 2014 Apr 29.

    Macronutrients and obesity: Revisiting the calories in, calories out framework.

    Riera-Crichton D1, Tefft N2.
    Author information

    Abstract
    Recent clinical research has studied weight responses to varying diet composition, but the contribution of changes in macronutrient intake and physical activity to rising population weight remains controversial. Research on the economics of obesity typically assumes a "calories in, calories out" framework, but a weight production model separating caloric intake into carbohydrates, fat, and protein, has not been explored in an economic framework. To estimate the contributions of changes in macronutrient intake and physical activity to changes in population weight, we conducted dynamic time series and structural VAR analyses of U.S. data between 1974 and 2006 and a panel analysis of 164 countries between 2001 and 2010.

    Findings from all analyses suggest that increases in carbohydrates are most strongly and positively associated with increases in obesity prevalence even when controlling for changes in total caloric intake and occupation-related physical activity.

    Our structural VAR results suggest that, on the margin, a 1% increase in carbohydrates intake yields a 1.01 point increase in obesity prevalence over 5 years while an equal percent increase in fat intake decreases obesity prevalence by 0.24 points.

  14. Paul the rat
    J Am Coll Nutr. 2014 Jun 9:1-5. [Epub ahead of print]

    Lessons from the War on Dietary Fat.

    Walker TB1, Parker MJ.
    Author information

    Abstract
    Conventional dietary guidelines put forth by health care institutions and providers for the past 40 years have stressed the importance of reducing the amount of dietary fat consumed. Such a diet is purported to mitigate metabolic risk factors and optimize the ability to achieve or maintain a healthy body weight. However, over the past 35 years obesity rates in the United States have risen dramatically though the level of dietary fat consumed by U.S. adults has fallen. This review examines the potential reasons for this paradox. Various meta-analyses, controlled trials, and cohort studies have demonstrated that reducing dietary fat intake provides for very little weight loss unless accompanied by equal or greater reductions in total energy intake. Due to both psychological (e.g., the tendency for people to eat more of what they consider low fat) and physiological (e.g., the low satiety that accompanies carbohydrate intake) factors, reducing total caloric intake while simultaneously reducing fat intake is a difficult challenge. Further, reductions in total carbohydrate intake, increases in protein intake, and adoption of a Mediterranean diet seem to be more effective in inducing weight loss than reductions in fat intake. Traditional claims that simply reducing dietary fat will improve metabolic risk factors are also not borne out by research. There is some evidence that replacing dietary saturated fat with unsaturated fat may improve metabolic risk factors, but that research is not conclusive. Teaching Points: • Over the past 40 years, Americans have decreased the percentage of calories they get from dietary fat while rates of overweight and obesity have risen dramatically. • It appears that a decrease in total dietary fat in ad libitum diets may induce a very small decrease in body weight. • Evidence suggests that reductions in total dietary fat intake often occur in conjunction with an increase in total caloric intake. •

    It seems reasonable to conclude that guiding the public to simply reduce dietary fat intake is an ineffective method to mitigate the rise in obesity and improve public health.

  15. Tina
    I vividly remember that when I was a kid (In Germany), we loved a liver sausage breadspread that came directly from the butcher. It was our most basic food - it always had (!) to be in the fridge. Every child I know loved it, and as toddlers you would lick it from the bread, and then push the bread aside or secretly throw it away. In all of our childhood it was one of the first learned (!) acts of discipline, not rejecting the bread any longer. It was considered naughty, indulgent and unhealthy to only eat the sausage (but it was all we really wanted). Now we know that organ meat is the most nutrient rich food that you can possibly get and that our instinct was absolutely spot on. Then, just a few years later "health conscious" mothers who believed in the food pyramid and the anti fat propaganda had banned this sausage completely and it was replaced with fat reduced margarine, fat reduced turkey breast or strawberry jam!!
  16. Paul the rat
    J Am Coll Nutr. 2014 Jul 2:1-7. [Epub ahead of print]

    Long-Term Effects of a Very Low-Carbohydrate Weight Loss Diet on Exercise Capacity and Tolerance in Overweight and Obese Adults.

    Wycherley TP1, Buckley JD, Noakes M, Clifton PM, Brinkworth GD.
    Author information

    Abstract
    Aim: Compare the long-term effects of an energy-restricted very low-carbohydrate, high-fat (LC) diet with an isocaloric high-carbohydrate, low-fat (HC) diet on exercise tolerance and capacity in overweight and obese adults. Methods: Seventy-six adults (25 males; age 49.2 ± 1.1 years; BMI 33.6 ± 0.5 kg/m2) were randomized to either a hypocaloric (6-7 MJ/day) LC diet (35% protein, 4% carbohydrate, 61% fat) or isocaloric HC diet (24% protein, 46% carbohydrate, 30% fat) for 52 weeks. Pre- and postintervention, participants' body weight and composition, handgrip, and isometric knee extensor strength were assessed and participants performed an incremental exercise test to exhaustion. Results: Forty-three participants completed the study (LC = 23; HC = 20). Overall, peak relative oxygen uptake increased (+11.3%) and reductions occurred in body weight (-14.6%), body fat percentage (-6.9% [absolute]), isometric knee extensor strength (-12.4%), handgrip strength (-4.5%), and absolute peak oxygen uptake (-5.2%; p ≤ 0.02 time for all) with no diet effect (p ≥ 0.18). During submaximal exercise, rating of perceived exertion did not change in either group (p = 0.16 time, p = 0.59 Time × Group). Compared to the HC diet, the LC diet had greater reductions in respiratory exchange ratio (LC -0.04 ± 0.01, HC -0.00 ± 0.01; p = 0.03), and increased fat oxidation (LC 15.0 ± 5.3% [of energy expenditure], HC 0.5 ± 3.9%; p = 0.04).

    Conclusion: In overweight and obese patients, an LC diet promoted greater fat utilization during submaximal exercise. Both an LC diet and an HC diet had similar effects on aerobic capacity and muscle strength, suggesting that long-term consumption of an LC weight loss diet does not adversely affect physical function or the ability to perform exercise.

  17. bill
    Paul the rat:

    Is there a place you've accumulated these studies?
    Or have I missed that?

    It would be wonderful if we could direct people to
    the studies you have posted.

    Reply: #19
  18. Paul the rat
    Hey bill,
    no I did not create a specific library for the papers I send to dietdoctor, I keep them with other papers in my own EndNote library. It is a good idea, maybe dietdoctor staff can create a References Folder for the citations we send.
    Reply: #21
  19. erdoke
    Here is an interesting follow-up on the relationship between special carbs in junk food (maltodextrins) and intestinal disbiosis:
    http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.01...
    The Dietary Polysaccharide Maltodextrin Promotes Salmonella Survival and Mucosal Colonization in Mice
  20. bill
    Thanks. I'd love to see such a link. You've
    offered up a wealth of information.

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