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Cardiac Disease, Carbohydrates and Weight Loss

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[edit] Diet and CAD

[edit] oxLDL (oxidized LDL) centered Prevention

  • Start off with this paper.

We know that oxLDL is a much better predictor of events than any score calculated from lipid panels. (see Tests_for_Preventative_Heart_Health#Oxidized_LDL_assay). Interventions based on lowering of oxLDL rather than the narrow focus on LDL appears to be the best bet. Normal LDL does not seem to be a risk other than it can become oxLDL. OxLDL is related to inflammation.

  • list of possible dietary interventions to lower oxLDL: 
Reduce postprandial BG to 110 Predictive Value of Circulating Oxidized LDL for Cardiac Events in Type 2 Diabetic Patients With Coronary Artery Disease
Quercetin
Lycopene
cocoa (non Dutched)
Olive oil
CoQ10 ?
Magnesium?
Soy Protein Isolate
DHEA
Vitamin D
L-Carnitine
Anthocyanins
Pomegranate 
Iodine
Reduce Iron
  • Might protect from oxLDL 
taurine (might protect from oxLDL)
Luteolin might protect Differential inhibition of oxidized LDL-induced apoptosis in human endothelial cells treated with different flavonoids 
ginseng - might protect
L-theanine (green tea) might protect?
vitamin d? 
reduce O-6 (block with fish oil)
  • Might increase 
Tryptophan might increase oxLDL http://www.sciencedirect.com/science/article/pii/002191509190254Z 
polunsaturated fats
Dietary oxChol - see next section!

[edit] Dietary Oxy Cholesterol

I think there is definite a red flag here - might explain the confusion with satFATS - satFats foods will often be refrigerated for some period - the longer the more oxy-CHOL. Particularly bad foods are powdered eggs, powdered milk - (dried whey protein ?) - these are found in all sorts of box food.. avoid those center isles.

...the quantity of oxidized lipids in their serum lipoproteins increased 16-fold and were significantly greater than in controls.

...in humans dietary oxidized lipids are absorbed by the small intestine, incorporated into chylomicrons, and appear in the bloodstream...

I think oxidized Cholesterol is probably connected to small Ldl - I don't understand this part yet.

oxidized lipids.. Sounds like modern beef is full of them - wish there was a study on grass-fed?

[edit] Cooking methods:

Looks like time is the critical factor - faster cooking is better.


[edit] Storage:

Powdered eggs? I think not.

This may be a good reason to modify a lowcarb diet to avoid oxidized cholesterol and may explain some of the inconsistencies of the earlier studies.

When I was on my failed lowfat diet for years I used a lot of "non-fat powdered milk" - did I do myself harm? (Thank you AHA)

I have these crazy questions that I keep thinking about - What changes have we made to our foods that have increased CAD?

What if freezing meat before cooking changes lipids in some way? Perhaps we are a lot better eating freshly butchered meats?


I'm thinking that OCP(Oxidized Cholesterol Products)(sometimes COPs) may help guide an optimal diet plan. I do remember that one of these studies caused McDs to change to vegetable oil for cooking their fries - keep lard hot all day and you do produce OCPs.

Meanwhile, it does appear that dietary sources of OCP increase atherosclerosis. I've identified 3 sources so far: powered milk, powdered eggs and beef. The powdered products are found in processed box foods - again pointing in the same direction. One study claimed that cholesterol in beef was almost 100% oxidized. (Again I'm wondering if it is really the beef or it is in fact that the modern industrial marbling cattle diet that has us not researching real beef, but sick beef in particular.) How I would like to see an NMR lipid profile and OCP numbers on grass fed vs fattened beef (even to look at 10 cattle).

[edit] Inflammation, Depression and CAD

[edit] Leptin resistance

[edit] Bacterial shower - Gut bacteria

Could be that the bacterial shower from eating food starts up an immune response that triggers systemic inflammation. Improving the gut barrier may be important.

  • Eating low-fat(AKA hi-carb) creates inflammation!

[edit] Wheat gluten and Inflammation

Gluten seems to be the inflammation culprit in wheat. Looks like a real link with heart disease:

If so, be aware that many of the lowcarb flour substitutes use gluten flour (sometimes denatured with heat). I wonder if that is the case for everyone or if it is like an allergy? - how would one test this - looks like we could test for anti-endomysial antibodies (AEA).

[edit] Serologic Tests for Celiac Disease

Antibody test Sensitivity (%) Specificity (%) Time course Cost*
IgA antiendomysial antibody 85 to 100 96 to 100 Antibody disappears within several months after institution of gluten-free diet. $45 to 99
IgA antitransglutaminase antibody 95 90 Limited data; correlated with IgA antiendomysial antibody in studies 85 to 164
IgA antigliadin antibody 53 to 100 65 to 100 More persistent than IgA antiendomysial antibody; may persist for 6 months or longer 45
IgG antigliadin antibody 57 to 100 42 to 98 Most persistent; may be detectable up to 12 months after institution of gluten-free diet
False-positive tests reported in patients with Crohn's disease, wheat-protein allergy, and post-diarrhea states

Sounds like "gliadin, a gluten protein" might be the problem Gluten is used as a stabilizing agent in products like ice-cream and ketchup, where it may be unexpected

Could it be that some people don't get the full blown Celiac Disease - but cause enough inflammation to cause heart problems?

Is it the gluten that causes small-LDL - or is it just inflammation?

[edit] The role of cytokines

[edit] Low Carb eating for heart health

[edit] Gary Taubs' Book Good Calories, Bad Calories

The 11 Critical Conclusions from Good Calories, Bad Calories:

  • Dietary fat, whether saturated or not, does not cause heart disease. [Not sure we know enough about all the types of sat-fat or the oxy-chol that often comes with it.]
  • Carbohydrates do, because of their effect on the hormone insulin. The more easily-digestible and refined the carbohydrates and the more fructose they contain, the greater the effect on our health, weight, and well-being.
  • Sugars—sucrose (table sugar) and high fructose corn syrup specifically—are particularly harmful. The glucose in these sugars raises insulin levels; the fructose they contain overloads the liver.
  • Refined carbohydrates, starches, and sugars are also the most likely dietary causes of cancer, Alzheimer’s Disease, and the other common chronic diseases of modern times.
  • Obesity is a disorder of excess fat accumulation, not overeating and not sedentary behavior.
  • Consuming excess calories does not cause us to grow fatter any more than it causes a child to grow taller.
  • Exercise does not make us lose excess fat; it makes us hungry.
  • We get fat because of an imbalance—a disequilibrium—in the hormonal regulation of fat tissue and fat metabolism. More fat is stored in the fat tissue than is mobilized and used for fuel. We become leaner when the hormonal regulation of the fat tissue reverses this imbalance.
  • Insulin is the primary regulator of fat storage. When insulin levels are elevated, we stockpile calories as fat. When insulin levels fall, we release fat from our fat tissue and burn it for fuel.
  • By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. By driving fat accumulation, carbohydrates also increase hunger and decrease the amount of energy we expend in metabolism and physical activity.
  • The fewer carbohydrates we eat, the leaner we will be.


[edit] GTT (Glucose Tolerance Test)

My father was an OB Gyn back when he lived in Wisconsin and used a 'glucose tolerance test' to check pregnant women for gestational diabetes. I remember him telling me that fasting blood sugar can miss diabetes - resulting in major problems for pregnant women. My father once had a Dr. Edgar Gordon as his endocrinology professor (UW) - the doctor who's 1963 JAMA diet article that inspired Dr. Atkins to write his variation. (My fasting sugar has always been fine and I've never had a 'glucose tolerance test' at a doctors office. In dealing with my reluctant doctor, I just ordered a case glucose and bought a cheap meter at Wall-mart - (total cost of $30 - less than a single lab fee!)).

See http://en.wikipedia.org/wiki/Glucose_tolerance_test

Because I had a whole case of glucola, I went ahead and tested my wife and daughter and found my wife had IGT(Impaired Glucose Tolerance) that our doctors fasting test missed. My wife has modified her diet (wish I could say the same for my daughter).

Why don't they do the 'glucose tolerance test'? Is it is too much of a hassle to have them come back in 2 hours? (reminds me of too much hassle to prescribe niacin because they might call about the flushing? Phone calls are a profit loss to doctors.)

When I was younger, I didn't think twice about eating sugar. Then I read some things that Dr Arthur Robinson Dr. Robinson (who was once a partner with Linus Pauling) wrote back in the late 90's and I decided to stop drinking any sugar drinks.

Today, I would not bother with the GTT - no one should be eating sugar - I just test my BG 1.5 to 2 hours after a meal - if it is over 110 I look at what and how much I ate and adjust my diet.

[edit] Fructose

I was wondering if fructose might be better than glucose (it was recommended for diabetics as a substitute for sugar) and did some more digging and reading and started wondering about HFCS and finally wrote Dr Robinson. He kindly wrote back telling me about an experiment he did on astronaut diet. They wanted a diet that produced no feces in space so they just consumed pure amino acids and pure sugars and some pure lipids. Everything worked out rather well, but the population complained of some boredom, so they replaced the glucose with fructose as a test. The result was high triglycerides. He also told me that fructose has a separate metabolic pathway compared to sugar.

We now know that fructose is a toxin:

Next paper pretty much settles any doubt:

After 10 weeks, the following differences were observed:
  • Intraabdominal fat: While both groups gained about 4 lbs on average, the glucose group increased intraabdominal fat (measured by abdominal CT scan) by 3.2%, fructose group by 14.0%
  • Small LDL: Glucose increased small LDL 13.3%; fructose increased small LDL 44.9%
  • Triglycerides: Contrary to several other observations, fasting triglycerides were no different between the two groups, but repeated assessment of triglyceride values (area under the cover) demonstrated 32% reduction with glucose, 99.2% increase with fructose.
  • Oxidized LDL: Increased 0.7% with glucose, increased 12.8% with fructose.
  • Postprandial (after-eating) triglyceride-rich remnant lipoproteins¾Increased 15.2% with glucose, increased 78.6% with fructose.

[edit] AGE (Advanced Glycation End-products)

Further reading over the years has convinced me that high blood sugars cause an increase in AGE(Advanced Glycation End-products). These plaques are involved in macular degeneration, Alzheimer disease, kidney disease, arthritis, and of course CAD. One other bit of information is that fructose is 10 times more likely to form AGE than glucose. I can imagine that even a slightly higher exposure to fructose (like that in HFCS) over a life time could lead to an increase in disease. Not all HFCS is the same - most is 55% fructose but there are some that are 60 to 65% fructose. The fructose in HFCS is not a disaccharides (as sucrose) and thus the fructose is circulated through the entire body before hitting the liver. Honey, often tauted as a health food, is pretty much a natural HFCS Honey, often erroneously tauted as a health food that it is NOT: 

   * 38.5% Fructose
   * 31.0% Glucose
   * 1.0% Sucrose (metabolizes to 50:50 glucose and fructose)
   * 9.0% (maltose (di - glucose), melezitose (a a nonreducing trisaccharide sugar))

It is also important to note that because fructose has a separate metabolic pathway compared to sugar that path way can become 'backed up' and I don't know that anyone is measuring blood-fructose levels that I know of (why not?). I have been told that the carbohydrate lobby has covertly and successfully blocked studies on the effects of HFCS.

Taubes book confirmed many of the things I found out by exhaustive Google scholar searches. One of that take home points is that our bodies will increase adipose tissue(fat tissue) to an amount that might be able to protect us from high blood sugars. If I want to lose weight - I need to reduce my insulin level. I don't think there is any other way - and that means limiting carbohydrates. Last year I started eating no sugar and no more than 12G of flour carbs in a day.

[edit] Glycemic Index

Not very useful - it is the area under the curve - time times the amount above 110 blood sugar that apparently counts. Being somewhat high for half a day is probably just as bad as being quite high for an hour. If one eats complex carbs then BG and insulin will be up for many hours and if ones insulin is up one CANNOT LOSE WEIGHT.

GI diets fool people into poor choices - Carbs should be reduced to keep postprandial sugars below 110 (use of an accurate meter is a must - most are not good enough). Don't fall for the low GI diet - it continues the carbohydrate addiction.

[edit] High Glycemic Dose

The high glycemic index dose will spike insulin and spike blood sugars for a relatively short time. Insulin will rise causing the body to store fat. High insulin levels are know to stimulate appetite (in fact insulin is sometimes given to anorexics to help get them to eat). Do the short but very high blood sugars cause major AGE damage?

[edit] Low Glycemic Dose

If the same 100G of glucose come bound in fiber and slowly absorbed - my body is exposed to slightly higher blood glucose levels for a long period of time. Slight insulin increases - that may prevent weight loss are experienced for a long time - perhaps preventing any release of triglycerides form adipose tissue and preventing weight loss?

I don't think there is a clear answer if Glycemic Index is useful - it may be that the form of the carbohydrates is more important? Might maltose vs galactose vs sucrose vs mono-saccharides as the form of carbohydrate be more important than glycemic index? What we need is some research to clear this up - and some research on the effects of the different di and mono saccharides. I'm not one to encourage government regulation, yet I think it is clear that if cigarettes need a warning label - so do sugar foods.

  • Good Calories, Bad Calories by Gary Taubes Does the medical establishment give good advise about obesity? Sounds like they are AWOL on this issue - the advice they are handing out not only fails to work, it is harming the public! Most of the commonly accepted truths of diet advice you think you know are probably wrong. Fat cells need insulin to grow - consuming carbohydrates - sugar, corn syrup, starch is what increases your insulin level. I would still exercise, but don't count on it helping you lose weight if you are eating refined carbohydrates. What the public needs to know was uncontroversial science in 1963 in a JAMA article by Dr. Edgar Gordon (UW endocrinologist). The public needs to understand that eating carbohydrates - particularly refined carbs (sugar, HFCS, flours) increases ones insulin level and that increase causes your body to store fat. You cannot lose weight with elevated insulin. The public also needs to know that the often parroted quote, "A calorie is a calorie", is simply wrong and is not supported by science. It also looks like sugars and flour cause colon cancer, not the lack of fiber. Sugars also cause high blood pressure, heart disease, stiffened collagen, older looking skin and possibly arthritis, Alzheimer's disease. If you only read one book on diet science, this should be it. The book is well referenced and clearly shows that the USA public diet information being disseminated is not based on science (as the experiments have never been done). Our public diet propaganda is based on a ‘trust and parrot’ attitude, and the idea that an expert’s opinion = science. Once again, we see that science + politics = BS. The book seemed a little repetitious towards the end, but well worth the struggle to read it.

[edit] Reducing homocystien


It looks like Homocysteine thiolactone is what causes CAD not homocysteine itself

According to: 

Hcy-thiolactone is detoxified by Hcy-thiolactonase/paraoxonase present in a subset of high-density lipoprotein particles in humans.

(should we be taking calcium?)


With that as a back ground - it appears that the methylation of homocystein happens with folic acid with the B12 enzyme. Polyenylphosphatidylcholine -> choline -> betane uses the BHMT(Betaine-Homocysteine Methyltransferase enzyme). So the question is: Pumping which system, BHMT or B12, is less likely to produce Homocysteine thiolactone?

It is possible that taking B vitamins and folic acid might do more harm than good.

Homocysteine metabol.png

[edit] Constipation

The lack of fiber isn't what causes constipation:


[edit] Related Pages

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