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Here's a new report which at least seems to support this claim (which is so common these days):
"A diet high in refined carbohydrates, like white rice or white bread, is associated with increased prostate tumor growth in mice.
Having too much insulin in the blood, a condition called hyperinsulinemia, is associated with poorer outcomes in patients with prostate cancer..."
Do you see the problem here? They are making it sound like any diet rich in "refined carbohydrates" (or as so many now say, "simple carbs") is problematic in this context. Let us leave aside the fact that this does not mean the tumor was caused by simple carbs, and focus instead on the fact that what they really found was that hyperinsulinemia is the problem. They then assumed that any diet rich in simple carbs causes this condition to occur. The reality appears to be very different, and Spindler's caloric restriction experiments showed (he found that the CR animals had an intense insulin spike when they ate, but that insulin levels went right back down to healthy levels). Thus, it may be the case that "complex carbs" are healthier in this one context at least, but only if you are eating a certain way ("the American way"). If you don't eat way too many calories, if you eat three meals a day only (spaced out evenly) with no other episodes of caloric intake, and if you eat enough high-quality protein (and don't eat too much UFAs or oxidized cholesterol), then it seems to be the case that "simple carbs" are fine, and won't cause the intestinal issues and won't have the anti-nutritive qualities that "complex carbs" do. I've certainly found this to be the case in my personal dietary experiments.
Source of the quoted material: http://www.sciencedaily.com/releases/2007/11/071127161824.htm |
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Once I saw a program on Japanese TV about a korean man living literally on junk "simple" carbohydrates. His refrigerator was full of HFCS soft drinks like Sprite and he always dined rice topped with chocolate. His hobby was badbington - a light sport and he was something over 60. When they did a blood test his markers looked like someone in his twenties...
About the spikes, they may be quite important to synchronize the clocks in the body. It has been shown that the cenetarians retain strong melatonin spikes during the daily sleep cycle while the people with chronic diseases have low melatonin and the expressions of their clock genes in different organs are out of sync.
Hans, I usually eat some sweet fruits like banana or apple in between the basic 3 meals a day, do you think this may be a problem? |
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Again, like you usually say, what is their definition of refined carbs? I know they say white bread and white flour, but do they also mean "French Fries" or "Donuts", which are also made with "white flour" but also fried in vegetable oil? I have noticed recently that vegetable oils, meaning cottonseed, soybean, peanut, canola, etc, are in almost every single "refined carbohydrate" product. Everything from cereals, to cakes, to muffins, donuts, to batters, to waffles, to everything else.
Are they controlling for this variable? Are they studying only fat free refined carbohydrates? |
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| Most such "studies" likely do not control for the fat content of such diets. As to eating between meals, I don't really know if it's better to eat more in three meals or to eat some fruit between the three meals (assuming you really need the calories). I would try to eat more calories during the three meals first, but if that didn't work I might want to go with four meals before eating fruit between the meals containing high-quality protein. If you try different things, post back here and tell us about your experiences. |
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| Some examples: Two relatives of mine have been overweight by quite a bit for more than a decade now. One is in his late 50s, the other is in her early 60s. He eats a lot of cooked meat, and a lot of calories in general. His lifestyle is very physical, much more so than the average American. She eats a lot of "simple carbs" and probably not enough high-quality protein, but probably a lot more PUFAs than is safe, as does he. |
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An interesting experimental study (not just a statistical review of available literature so common these days):
South Med J. 1988 Jan;81(1):61-3.
Reducing the serum cholesterol level with a diet high in animal fat.
Newbold HL.
Multiple food allergies required a group of seven patients with elevated serum cholesterol levels to follow a diet in which most of the calories came from beef fat. Their diets contained no sucrose, milk, or grains. They were given nutritional supplements. This is the only group of people in recent times to follow such a diet. During the study, the patients' triglyceride levels decreased from an average of 113 mg/dl to an average of 74 mg/dl; at the same time, their serum cholesterol levels fell from an average of 263 mg/dl to an average of 189 mg/dl. At the beginning of the study, six of the patients had an average high-density lipoprotein percentage of 21%. At the end of the study, the average had risen to 32%. These findings raise an interesting question: are elevated serum cholesterol levels caused in part not by eating animal fat (an extremely "old food"), but by some factor in grains, sucrose, or milk ("new foods") that interferes with cholesterol metabolism?
PMID: 3336803 |
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| Ray Peat talked about dietary PUFAs interfering with cholesterol metabolism. What I dislike about these kinds of studies is that they use a diet hardly anyone will follow for more than a short period of time. |
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The following makes the "sugar problem" much clearer to me finally. The problem is not sugar or intrinsically insulin but carbohydrate consumption beyond the point when the body starts makig storage fat from it.
Too Much Sugar Kills Your Sex Life
High levels of sugar in your bloodstream can turn off the gene that controls your sex hormones.
The simple sugars, glucose and fructose, are metabolized in your liver, with the excess stored as fat lipids. Excess fat synthesis deactivates your SHBG (sex hormone binding globulin) gene, causing your levels of SHBG protein to drop dramatically, and it is this SHBG protein that controls your testosterone and estrogen levels.
Too little SHBG protein means your body will produce too much testosterone and estrogen, which increases your chances of acne, infertility, polycystic ovaries, uterine cancer, and heart disease.
Said Dr. Geoffrey Hammond, lead researcher, “We discovered that low levels of SHBG in a person’s blood means the liver’s metabolic rate is out of whack �?because of inappropriate diet or something that ‘s inherently wrong with the liver �?long before there are any disease symptoms.�?BR>
This new study also challenges the previous conventional thought that high levels of insulin are to blame for the drop in SHBG, and that it’s actually the liver’s metabolism of sugar that counts.
Sources:
Physorg.com November 10, 2007
Softpedia November 10, 2007
The Journal of Clinical Investigation November 8, 2007, Epub Ahead of Print (Free Full Text Report) |
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Here's a post I did to another newsgroup, with a main point being that it is getting some press coverage, despite the flaws:
For example: "Low-carb Diet Reduces Inflammation And Blood Saturated
Fat In Metabolic Syndrome."
Source:http://www.sciencedaily.com/releases/2007/12/071203091236.htm
But when you look at the actual study (or, in this case, the
abstract), you find that the "low fat" diet was 24% fat ! The "low
fat" group also ate much less protein (28% vs. 20%). And we are not
told (in the abstract) what the sources of fat were, which can make
all the difference, since inflammatory molecules are made from fatty
acids, not carbohydrates.
One off the researchers is quoted as saying:
"The real importance of diets that lower carbohydrate content is that
they are grounded in mechanism -- carbohydrates stimulate insulin
secretion which biases fat metabolism towards storage rather than
oxidation. The inflammation results open a new aspect of the
problem..."
First of all, the diet was fed for 12 weeks, so if that's all you want
to live, then fine, but otherwise, it's obviously too short a term for
humans to worry about, whatever the results were. On a diet of 5% or
less fat, coming from fresh coconut oil mostly, the results would be
totally different (though it would have to be much longer than a 12
week study, due to the changeover from AA to Mead acid, which takes at
least approximately 2 years). Secondly, in general, if you have a
great deal of fatty acid oxidation, you are going to have more free
radical damage to vital biomolecules, but again, it would take a lot
more than 12 weeks to see the effects of such damage. Thirdly, there
is an obvious non sequitur in this statement; the person seems to
think there is a necessary connection between insulin secretion and
"inflammation" (leaving aside the fact that chronic inflammation of
unknown origin is only possible with AA in your cells).
Calorie-restriction researcher Dr. Spindler found, for instance, that
his CR animals experience an intense an beneficial insulin spike
during meals. The insulin "comes and goes" quickly, not doing any
damage, not becoming "resistant," and apparently doing an excellent
job of recycling vital biomolecules. What does "inflammation" (what
they actually mean are "markers" of "inflammation") have to do with
this? Note that in their own abstract they state clearly: "Both diets
significantly decreased the concentration of several serum
inflammatory markers..." And what were the subjects' diets like
before the study? All we are told in the abstract is that these
people were: "Overweight men and women with atherogenic
dyslipidemia." Thus, they choose people with obvious dietary issues
and fed them low calorie diets (1504 or 1478 kcal).
I would characterize this "study" as a near total "mess," and more of
a study of calorie restriction (many of the subjects were likely
consuming at least 3000 kcal per day before the study) than anything
else, but again, the time period studied is too short term to know
what the long term effects would be from either of these "CR" diets.
The abstract of the study is:
Abnormal distribution of plasma fatty acids and increased inflammation
are prominent features of metabolic syndrome. We tested whether these
components of metabolic syndrome, like dyslipidemia and glycemia, are
responsive to carbohydrate restriction. Overweight men and women with
atherogenic dyslipidemia consumed ad libitum diets very low in
carbohydrate (VLCKD) (1504 kcal:%CHO:fat:protein = 12:59:28) or low in
fat (LFD) (1478 kcal:%CHO:fat:protein = 56:24:20) for 12 weeks. In
comparison to the LFD, the VLCKD resulted in an increased proportion
of serum total n-6 PUFA, mainly attributed to a marked increase in
arachidonate (20:4n-6), while its biosynthetic metabolic intermediates
were decreased. The n-6/n-3 and arachidonic/eicosapentaenoic acid
ratio also increased sharply. Total saturated fatty acids and 16:1n-7
were consistently decreased following the VLCKD. Both diets
significantly decreased the concentration of several serum
inflammatory markers, but there was an overall greater anti-
inflammatory effect associated with the VLCKD, as evidenced by greater
decreases in TNF-alpha, IL-6, IL-8, MCP-1, E-selectin, I-CAM, and
PAI-1. Increased 20:4n-6 and the ratios of 20:4n-6/20:5n-3 and n-6/n-3
are commonly viewed as pro-inflammatory, but unexpectedly were
consistently inversely associated with responses in inflammatory
proteins. In summary, a very low carbohydrate diet resulted in
profound alterations in fatty acid composition and reduced
inflammation compared to a low fat diet.
Lipids. 2007 Nov 29 [Epub ahead of print].
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView... |
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I think the problem here is that the carbs can "overflow" the fat storage cells while protein or fat cannot do this. Or perhaps we can ingest unlimited amounts of carbs while too much protein or fat would make us sick. The fat cells bursting from overload are then the irritant which starts the inflammatory cascade. Other unrelated irritants are e.g. AGEs/ALEs or uric acid crystals. I came to the conclusion that sugar consumption is safe as far as the fat storage cells (adipocytes) are not completely filled with the storage fat. This is my post I also made on the other group:
It has become apparent that the evolution did not think wisely about
the design after the reproductive age is over so that our aging just
represents the developmental program run abruptly overtime. Another miss is that the evolution has not predicted that we may ever run into carbohydrate overfeeding lasting longer than a few weeks in the summer. In the early forming days carbohydrates were scarce and present mostly in root vegetables. Thus the evolution made every effort to make energy reserves from them (e.g. giving us multiple copies of the amylase genes) not bothering to create a regulatory mechanism to stop "filling the tanks" when they are full (because they apparently never got full). The novaday lifestyle represents continuous carbohydrate excess combined with sedentary lifestyle so the tanks are always being filled and "never" taken from unless people live physically active lifestyle. The "tanks" are called adipocytes and when they cannot take more volume of fuel (fat) which is being pushed into them by the "harsh biochemical forces" they just burst open. This is of course sensed by the body as a damage and an inflammatory repair response is mounted. Because the feeding and adipocyte bursting keep going on the inflammatory response never has chance to finish its job and is struck in the original "destructive" phase resulting in the well known chronic systemic inflammation. Following are some citations describing the inflammatory response against the irritant (bursting adipocytes overloaded with fat made from sugar). If we could develop a sensor telling how much fuel we have in our tanks we could prevent many of the chronic diseases of today. At least the evolution gave us the brains so that we can construct one. Unfortunately, the medical establishment is rather interested in suppressing the consequences with inhibitors of the inflammatory response like NSAIDS rather than making such sensor. And
the food industry keeps feeding us the cheap carbs in excess as well as providing other nutrient/mineral depleted food which makes us hungry even more ...
Taka
P.S.: Of course it's not as simple as this as there are other factors
in play such as PUFAs inhibiting the basal metabolism (via thyroid)
which can burn some of the extra carbs before they are put into the
storage.
J Clin Invest. 2007 Jan;117(1):175-84.
Obesity induces a phenotypic switch in adipose tissue macrophage
polarization.
Lumeng CN, Bodzin JL, Saltiel AR.
Life Sciences Institute, University of Michigan, Ann Arbor, Michigan
48109, USA.
Adipose tissue macrophages (ATMs) infiltrate adipose tissue during
obesity and contribute to insulin resistance. We hypothesized that
macrophages migrating to adipose tissue upon high-fat feeding may
differ from those that reside there under normal diet conditions. To
this end, we found a novel F4/80(+)CD11c(+) population of ATMs in
adipose tissue of obese mice that was not seen in lean mice. ATMs from
lean mice expressed many genes characteristic of M2 or "alternatively
activated" macrophages, including Ym1, arginase 1, and Il10. Diet-
induced obesity decreased expression of these genes in ATMs while
increasing expression of genes such as those encoding TNF-alpha and
iNOS that are characteristic of M1 or "classically activated"
macrophages. Interestingly, ATMs from obese C-C motif chemokine
receptor 2-KO (Ccr2-KO) mice express M2 markers at levels similar to
those from lean mice. The antiinflammatory cytokine IL-10, which was
overexpressed in ATMs from lean mice, protected adipocytes from TNF-
alpha-induced insulin resistance. Thus, diet-induced obesity leads to
a shift in the activation state of ATMs from an M2-polarized state in
lean animals that may protect adipocytes from inflammation to an M1
proinflammatory state that contributes to insulin resistance.
PMID: 17200717
J Lipid Res. 2005 Nov;46(11):2347-55. Epub 2005 Sep 8.
Adipocyte death defines macrophage localization and function in
adipose tissue of obese mice and humans.
Cinti S, Mitchell G, Barbatelli G, Murano I, Ceresi E, Faloia E, Wang
S, Fortier M, Greenberg AS, Obin MS.
Institute of Normal Human Morphology, University of Ancona, Ancona,
Italy.
Macrophage infiltration of white adipose tissue (WAT) is implicated in
the metabolic complications of obesity. The precipitating event(s) and
function(s) of macrophage infiltration into WAT are unknown. We
demonstrate that >90% of all macrophages in WAT of obese mice and
humans are localized to dead adipocytes, where they fuse to form
syncytia that sequester and scavenge the residual "free" adipocyte
lipid droplet and ultimately form multinucleate giant cells, a
hallmark of chronic inflammation. Adipocyte death increases in obese
(db/db) mice (30-fold) and humans and exhibits ultrastructural
features of necrosis (but not apoptosis). These observations identify
necrotic-like adipocyte death as a pathologic hallmark of obesity and
suggest that scavenging of adipocyte debris is an important function
of WAT macrophages in obese individuals. The frequency of adipocyte
death is positively correlated with increased adipocyte size in obese
mice and humans and in hormone-sensitive lipase-deficient (HSL-/-)
mice, a model of adipocyte hypertrophy without increased adipose mass.
WAT of HSL-/- mice exhibited a 15-fold increase in necrotic-like
adipocyte death and formation of macrophage syncytia, coincident with
increased tumor necrosis factor-alpha gene expression. These results
provide a novel framework for understanding macrophage recruitment,
function, and persistence in WAT of obese individuals.
PMID: 16150820 |
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| I need to see specific diets tested against other specific diets, and for a lot more than 2 weeks (probably about half a year should be the minimum). With all the factors not controlled in these kinds of "studies," just about any results are possible. The way the "media" presents these studies to the public, however, is another issue entirely, and one that is quite interesting, at least to me. |
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QUOTE: Red wine has been shown to protect people from heart disease, even when they follow a diet high in saturated fat, and the healing powers of tea are becoming the stuff of legend. Now, researchers at the University of Massachusetts Amherst have shown that these beverages may hold promise for regulating the blood sugar of people with type 2 diabetes...
Diabetes places a stress on the entire body by increasing the production of free radicals, including molecules that react with oxygen, which degrade cellular function. Both red wine and tea contain antioxidants with proven health benefits, and have the potential to manage heart disease, high blood pressure and perhaps contribute to the prevention of cancer, which are all linked to free radicals.
“These results provide strong evidence for further studying the use of wine and tea to manage some stages of type 2 diabetes using animal models and clinical studies, and point to the importance of an antioxidant-rich diet as part of an overall management strategy,�?says Shetty. “This concept is not new, but we are finding clear cellular targets for the functions of dietary polyphenolics. Using specific beverage combinations could generate a whole food profile that has the potential to manage type 2 diabetes and its complications, especially in the early stages.�? UNQUOTE.
Source: http://www.sciencedaily.com/releases/2008/04/080402212428.htm
My comment: Of course, what we see here is perhaps the major problem in the context of preventing chronic disease by diet, that is, free radical damage/activity is recognized as the underlying cause or a huge factor, but "saturated fat" gets blamed, even though saturated fatty acids do not contribute to free radical activity or "inflammation," and in fact may serve to lessen it (depending upon the exact situation).
However, because "nutritional experts" classified food items such as lard as "saturated fat" (even though it is only about 40% saturated fatty acids, and therefore very subject to free radical attack, known as lipid peroxidation), there is such confusion that coconut oil, which is about 92% saturated fatty acids (and therefore is not problematic in the lipid peroxidation/free radical generation context), is classified as a "saturated fat" and also blamed for all kinds of ill health.
Of course, if this were true, Asian nations on coconut rich diets would have huge rates of heart disease, diabetes, etc., when in fact the opposite is the case (until they start consuming diets rich in unsaturated fatty acids, which are a huge problem, especially in the form of highly refined oils that are then used to cook with while exposed to air). |
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The newest threads on the AGE/ALE on the Hyperlipid Blog are worth reading:
http://high-fat-nutrition.blogspot.com/2008/07/age-rage-and-ale-ale-of-ldl.html
The final conclusion is that "sugar is what oxidises the PUFA in LDL to give oxLDL" and here is the relevant Abstract to back it up:
Proc Natl Acad Sci U S A. 1993 Jul 15;90(14):6434-8.
Lipid advanced glycosylation: pathway for lipid oxidation in vivo.
Bucala R, Makita Z, Koschinsky T, Cerami A, Vlassara H.
Picower Institute for Medical Research, Manhasset, NY 11030.
To address potential mechanisms for oxidative modification of lipids in vivo, we investigated the possibility that phospholipids react directly with glucose to form advanced glycosylation end products (AGEs) that then initiate lipid oxidation. Phospholipid-linked AGEs formed readily in vitro, mimicking the absorbance, fluorescence, and immunochemical properties of AGEs that result from advanced glycosylation of proteins. Oxidation of unsaturated fatty acid residues, as assessed by reactive aldehyde formation, occurred at a rate that paralleled the rate of lipid advanced glycosylation. Aminoguanidine, an agent that prevents protein advanced glycosylation, inhibited both lipid advanced glycosylation and oxidative modification. Incubation of low density lipoprotein (LDL) with glucose produced AGE moieties that were attached to both the lipid and the apoprotein components. Oxidized LDL formed concomitantly with AGE-modified LDL. Of significance, AGE ELISA analysis of LDL specimens isolated from diabetic individuals revealed increased levels of both apoprotein- and lipid-linked AGEs when compared to specimens obtained from normal, nondiabetic controls. Circulating levels of oxidized LDL were elevated in diabetic patients and correlated significantly with lipid AGE levels. These data support the concept that AGE oxidation plays an important and perhaps primary role in initiating lipid oxidation in vivo.
PMID: 8341651 |
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Have you read the evidence I posted in the general forum, in the thread entitled: Glycation's role in "disease" and "aging." ?
There is one study that is particularly good:
THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 271, No. 17, Issue of April
26, pp. 9982-9986, 1996
© 1996 by The American Society for Biochemistry and Molecular Biology,
Inc. Printed in U.S.A.
"The Advanced Glycation End Product, Ne-(Carboxymethyl)lysine, Is
a Product of both Lipid Peroxidation and Glycoxidation Reactions*"
QUOTE: "CML is also formed during
metal-catalyzed oxidation of polyunsaturated fatty
acids in the presence of protein... We also report that CML, heretofore
described as a gly-coxidation
product, is formed during peroxidation of polyunsat-urated
fatty acids (PUFA) in the presence of ribonuclease A (RNase), a protein
that contains neither enzymatically nor
nonenzymatically attached carbohydrate... oxidation of fatty acid is
clearly a more efficient source of CML, despite the fact that the
glucose is in solution throughout the course of the experiment,
while the PUFA are only progressively solubilized. Further,
after 6 days of incubation, a large fraction of the arachidonate
was oxidized based on its solubilization in the aqueous phase,
while 2% of the glucose is oxidized during this same time
period... The observations described above indicate that CML,
previ-ously
described as a glycoxidation product or AGE, may, in fact,
be derived from PUFA during lipid peroxidation reactions. UNQUOTE. |
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