Cardiac Disease, Carbohydrates and Weight Loss


Diet and CAD

oxLDL (oxidized LDL) centered Prevention

We know that oxLDL is a much better predictor of events than any score calculated from lipid panels. (see Tests_for_Preventative_Heart_Health- see 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.

L-Carnitine
Anthocyanins
Pomegranate 
Quercetin
Lycopene
cocoa (non Dutched)
Iodine
CoQ10 ?
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?
 :* 
Tryptophan might increase oxLDL http://dx.doi.org/10.1016/0021-9150(91)90254-Z
Dietary oxChol - see next section!

Excess PUFA

One bit that the public is not aware of is that between 1960 and today, the amount of PUFA's (Poly Unsaturated Fats) in our diets has increased 5x - this is a result of breeding frost resistant strains - this corn, soy and wheat accounts for most of the carbon in our food supply. The problem is too much PUFA is not good for us. It causes a lot of people to get fat and produces systemic inflammation - which leads to things like CAD, depression, joint pain, and a list of other health problems.

I can look at my old high-school pictures (1970s) and we were not over weight. If you look at high-school kids today, you will see that more than half are now over weight. This is likely a result of the increased PUFA's and sugar in the diet ( the combination is REALLY bad).

Excess PUFAs interfere with insulin-blood-glucose regulation.

Fish oils block some of the bad effects of PUFA - but not all - best to avoid all vegetable oil based foods - corn fed chicken and eggs tend to be high . there is beef, fish etc.

Vegan Vegetarian risks

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?

Cooking methods:

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


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. 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).

Inflammation, Depression and CAD

Leptin resistance

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.

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).

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?

The role of cytokines

Low Carb eating for heart health

Gary Taubs' Book Good Calories, Bad Calories

The 11 Critical Conclusions from Good Calories, Bad Calories:


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?

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.

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.

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.

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.

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?

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.

Reducing homocystien

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 it possible that taking B vitamins and folic acid might do more harm than good?

Homocysteine metabol.png

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