The heart that is able to make calls in case of an emergency | NextScience.org
Carbohydrate restriction is effective in improving atherogenic dyslipidemia even in the absence of weight loss -- Westman et al. 84 (6): 1549 -- American Journal of Clinical Nutrition
"Given how difficult it is to lose weight, the data of Krauss et al support the notion that carbohydrate restriction is the default diet for treatment of atherogenic dyslipidemia. Because low-carbohydrate strategies are at least as effective at fat reduction as are low-fat diets, it is reasonable to conclude that carbohydrate restriction, lower or higher in SFA, is the preferred diet for most people and especially those with the complex of health markers referred to as metabolic syndrome, as we previously suggested (10)."

Interesting critique of Krauss' timid, if not misleading discussion of his remarkable results that low carb diet reduced heart disease risk. Glaring point: that the benefits of low carb not improved after weight loss is pointed out. Of course not! The improvement has already occurred. By time weight loss achieved IN THESE SUBJECTS the benefits have been achieved. All subjects in study lost weight and once they lost weight there were less further improvements. Not the same as saying a thin subject wouldn't also yield improvements once on low carb diet. Very confusing of Kauss. What's he hiding from?
Carbohydrate restriction is effective in improving atherogenic dyslipidemia even in the absence of weight loss -- Westman et al. 84 (6): 1549 -- American Journal of Clinical Nutrition
Addition of glucose to an oral fat load reduces postprandial free fatty acids and prevents the postprandial increase in complement component 3 -- van Oostrom et al. 79 (3): 510 -- American Journal of Clinical Nutrition
Mix It Up: No Need To Separate Foods During Meals - SkylerTanner.com
Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia -- Krauss et al. 83 (5): 1025 -- American Journal of Clinical Nutrition
Note that increased physical activity without dietary carbohydrate reduction can also result in improvements in the components of atherogenic dyslipidemia (30) and can have the additional benefit of helping to maintain reductions in body weight.
JAMA -- Abstract: Association of small low-density lipoprotein particles with the incidence of coronary artery disease in men and women, September 18, 1996, Gardner et al. 276 (11): 875
LDL size was significantly smaller in CAD cases than in controls in a prospective, population-based study. These findings support other evidence of a role for small, dense LDL particles in the etiology of atherosclerosis.
Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia -- Krauss et al. 83 (5): 1025 -- American Journal of Clinical Nutrition
"Krauss RM"[Author] - PubMed Results
Scanner to Find Fatty Deposits in Vessels Is Approved - New York Times
Federal regulators have approved the sale of a new laser scanning system intended to locate fatty deposits in blood vessel walls that are thought to cause heart attacks.
Food effects on Insulin levels
Not sure where these charts came from, so reader beware. Interesting if accurate. Might be from Protein Power of Michael Eades.
Does Exercise Really Make Us Thinner? -- New York Magazine
Letter On Corpulence by William Banting -
Vegetarians Live Longer: Results of 25-Year Vegetarians Study of the Deutsches Krebsforschungszentrum (German Cancer Research Center)
"Comparing these three categories, occasional meat consumers seem to have opted for the healthiest diet, i.e. the observed lowered mortality risk cannot be attributed to complete abstention from meat and fish."

"[Note by Healing Cancer Naturally: I suggest that the greater vitality of those occasionally partaking of meat or fish is not attributable to any particularly health-promoting ingredients in these items not encountered in other edibles, but rather to a more relaxed and less dogmatic attitude likely to be more prevalent in this particular dietary group.]"

BZ - How's that for an ad hoc hypothesis? Jeez...
The origins of western obesity: a role for animal ...[Med Hypotheses. 2000] - PubMed Result
Although dietary protein by itself provokes relatively little insulin release, it can markedly potentiate the insulin response to co-ingested carbohydrate; Western meals typically unite starchy foods with an animal protein-based main course. Thus, postprandial insulin secretion may be reduced by either avoiding animal protein, or segregating it in low-carbohydrate meals; the latter practice is a feature of fad diets stressing 'food combining'. Vegan diets tend to be relatively low in protein, legume protein may be slowly absorbed, and, as compared to animal protein, isolated soy protein provokes a greater release of glucagon, an enhancer of fat oxidation. The low insulin response to rice may mirror its low protein content. Minimizing diurnal insulin secretion in the context of a low fat intake may represent an effective strategy for achieving and maintaining leanness.
Health & Nutrition by Michael R. Eades, M.D. » Jack LaLanne vs Ancel Keys

Health & Nutrition by Michael R. Eades, M.D. » A bad week for statins
Krajčovičová-Kudláčková et al.
Advanced glycation end products (AGEs) may play an important adverse role in process of atherosclerosis, diabetes, aging and chronic renal failure. Levels of Ne-carboxymethyllysine and fluorescent AGE values were estimated in two nutritional population groups - alternative group (vegetarians - plant food, milk products, eggs) and traditional group (omnivorous subjects). Vegetarians have a significantly higher carboxymethyllysine content in plasma and fluorescent AGE values. Intake of proteins, lysine and monosaccharides as well as culinary treatment, consumption of food AGEs (mainly from technologically processed products) and the routes of Maillard reaction in organism are the substantial sources of plasma AGEs. Vegetarians consume less proteins and saccharides. Lysine intake is significantly reduced (low content in plant proteins). Subjects on alternative nutrition do not use high temperature for culinary treatment and consume low amount of technologically processed food. Fructation induced AGE fluorescence is greater as compared with that induced by glucose. It is due to higher participation of a more reactive acyclic form of fructose. Intake of vegetables and fruit with predominance of fructose is significantly higher in vegetarians. Comparison of nutrition and plasma AGEs in vegetarian and omnivorous groups shows that the higher intake of fructose in alternative nutrition of healthy subjects may cause an increase of AGE levels.
WHFoods: Shrimp
In a peer-reviewed scientific study, researchers looked at the effect of two diets, one which contained shrimp and the other eggs, on the cholesterol levels of people with normal lipid levels. In this randomized crossover trial, people ate either 300 grams of shrimp per day or two large eggs. (A randomized crossover trial is one in which groups cross over, trying out both possible protocols.) The shrimp diet did raise LDL levels (bad cholesterol) by 7%, but also raised HDL levels (good cholesterol) by 12%. In contrast, the egg diet raised LDL levels by 10% and HDL by 7%. The results then showed that the shrimp diet produced significantly lower ratios of total to HDL ("good") cholesterol and lower ratios of LDL ("bad" cholesterol) to HDL cholesterol than the egg diet. In addition, in people who ate the shrimp diet, levels of triglycerides (a form in which fat is carried in the blood) decreased 13%.
Scientists Find Blueberries Reverse Age Related Memory Deficits
Phytochemical-rich foods, such as blueberries, are not only healthy food choices, they may actually be able to reverse age-related memory problems. That's the conclusion of a study by a research team from the University of Reading and the Peninsula Medical School in England.
The Eat to Live Six Week Program
Dr. Galland's Integrated Medicine - Leo Galland M.D., F.A.C.N. - HealthWorld Online
Fat resistence diet article - Breakthrough Science
Health and Nutrition Article - The Five Rules for Mastering Leptin - The Hunger Hormone
There is science and good sense behind each rule.

Rule 1: Never eat after dinner. Finish eating 3 hours before bedtime. Never go to bed on a full stomach. Allow 11-12 hours between dinner and breakfast. For approximately the first 6-8 hours after eating our evening meal, the body is burning up the calories from that day. The most effective fat burning time (i.e. stored fat in our thighs, bums and tums) is between approximately 8 and 12 hours after eating. If we have a little snack before bedtime, or have our evening meal too late, the leptin tells the brain that no energy is required, and no fat burning will occur in the latter part of the night. So that little snack, however healthy it may have been, puts paid to any fat-burning that night.

Rule 2: Eat 3 meals per day. Allow 5-6 hours between meals. Do Not Snack. During the first three hours after a meal, insulin is in charge of storing the calories from the food we have eaten. During this time we are not in 'fat-burning mode'. Even low-calorie snacks stimulate insulin release.

If you find it too difficult to wait 5 hours before eating, then you can start this plan by eating four meals per day, instead of three. In time, with regular exercise added, you will more and more often be able to leave 5 hours between meals. The most important time is the night-time 11-12 hour fat-burning interval.

Children and teenagers of normal weight, athletes and bodybuilders will probably need to eat more often than three times per day. However, try to avoid unhealthy snacks or fizzy drinks.

Rule 3: Do not eat large meals. The idea behind this is to not give the body more fuel than it can use. Regular large meals leads to leptin and insulin resistance. One of the best techniques for reducing the size of meals is to eat slowly and chew really well. It takes the brain ten minutes to realise you are full. If you really can't slow down, then put down your knife and fork for 5 minutes when you've eaten about half your food. Don't feel you have to 'clean your plate' if you have had enough - you becoming overweight and unhealthy doesn't help anyone.

Rule 4: Eat a high-protein breakfast. This keeps the body in a calorie-burning mode. Eating a protein breakfast supports blood sugar levels so that late afternoon energy crashes are minimised. These energy crashes are often the result of eating a breakfast with too many carbohydrates and very little protein. If you eat a high carbohydrate breakfast, and are leptin resistant, you are more likely to overeat generally, but particularly at night.

Rule 5: Reduce the amount of carbohydrate eaten. This does NOT mean cutting out all, or virtually all, carbohydrates. We do need carbohydrates to maintain health.

Health and Nutrition Article - The Five Rules for Mastering Leptin - The Hunger Hormone
Cholesterol, Heart Disease : Active Low-Carber Forums
Insulin and Its Metabolic Effects by Ron Rosedale, M.D.
It has actually been shown by quite a number of papers that resistance training for insulin resistance is better than aerobic training. There are a variety of other reasons too. Resistance training is referring to muscular exercises. If you just do a bicep curl, you immediately increase the insulin sensitivity of your bicep. Just by exercising, and what you are doing is you are increasing the blood flow to that muscle. That is one of the factors that determines insulin sensitivity is how much can get there. It has been shown conclusively that resistance training will increase insulin sensitivity.
L-lysine content in foods. Composition from lowest to highest l-lysine quantity amount.
100% (1.00) amount represents equal amounts of amino acids L-lysine and L-arginine (sometimes called also L-arganine) in a food. A number above the 100% (1.00) mark means the food contains higher amount of L-lysine, therefore it is richer in l-lysine content. In contrary, any number below the 100% (1.00) mark represents higher amount of L-arginine in the food.
Amazon.com: Why Animals Don't Get Heart Attacks but People Do, Fourth Revised Edition: Matthias Rath: Books
L-Lysine also plays another important roll in the repair process. It binds onto Lipo-Protein A. (Lp(a))which our liver makes as a response to cracked arteries nullifying its stickiness thus halting the build up of plaques.Lp(a)is a component of our LDL colesterol but they dont even check for it in normal collesterol checks.
DoctorYourself.com - Health, Naturally!
Insulin and Its Metabolic Effects by Ron Rosedale, M.D.
I mentioned that insulin increases cellular proliferation, what does that do to cancer? It increases it. And there are some pretty strong studies that show that one of the strongest correlations to breast and colon cancer are with levels of insulin.
Insulin and Its Metabolic Effects by Ron Rosedale, M.D.
If you drip insulin into the artery of a dog, there was a Dr. Cruz who did this in the early 70's by accident, he was doing a diabetic experiment and found out that the femoral artery that the insulin was being dripped into was almost totally occluded with plaque after about three months.

The contra lateral side was totally clear, just contact of insulin in the artery caused it to fill up with plaque. That has been known since the 70's, it has been repeated in chickens, in dogs, it is really a well-known fact. Insulin floating around in the blood causes a plaque build up. They didn't know why, but we know that insulin causes endothelial proliferation, that's the first step, it causes a tumor, an endothelial tumor.
Insulin and Its Metabolic Effects by Ron Rosedale, M.D.
What is the purpose of insulin? As I mentioned, in some organisms it is to control their lifespan, which is important. What is the purpose of insulin in humans? If you ask your doctor, they will say that it's to lower blood sugar and I will tell you right now, that is a trivial side effect. Insulin's evolutionary purpose, among others at least known right now, we are looking at others, is to store excess nutrients.
Insulin and Its Metabolic Effects by Ron Rosedale, M.D.
But if we know that vitamin C and glucose have similar chemical structure, what happens when the sugar levels go up? They compete for one another upon entering the cells. And the thing that mediates the entry of vitamin C into the cells is the same thing that mediates the entry of glucose into the cells. If there is more glucose around there is going to be less vitamin C allowed into the cell and it doesn't take much. A blood sugar value of 120 reduces the phagocytic index seventy-five percent.
Insulin and Its Metabolic Effects by Ron Rosedale, M.D.
YouTube - How Does Leptin Impact Your Level of Health?

YouTube - Exposing the Cholesterol Myth
Dr. Ron Rosedale talks about common cholesterol myths.

Plant- and marine-derived n-3 polyunsaturated fatt...[Am J Clin Nutr. 2003] - PubMed Result
BACKGROUND: Dietary alpha-linolenic acid (ALA) can be converted to long-chain n-3 polyunsaturated fatty acids (PUFAs) in humans and may reproduce some of the beneficial effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on cardiovascular disease risk factors. OBJECTIVE: This study aimed to compare the effects of increased dietary intakes of ALA and EPA+DHA on a range of atherogenic risk factors. DESIGN: This was a placebo-controlled, parallel study involving 150 moderately hyperlipidemic subjects randomly assigned to 1 of 5 interventions: 0.8 or 1.7 g EPA+DHA/d, 4.5 or 9.5 g ALA/d, or an n-6 PUFA control for 6 mo. Fatty acids were incorporated into 25 g of fat spread and 3 capsules to be consumed daily. RESULTS: The change in fasting or postprandial lipid, glucose, or insulin concentrations or in blood pressure was not significantly different after any of the n-3 PUFA interventions compared with the n-6 PUFA control. The mean (+/- SEM) change in fasting triacylglycerols after the 1.7-g/d EPA+DHA intervention (-7.7 +/- 4.99%) was significantly (P < 0.05) different from the change after the 9.5-g/d ALA intervention (10.9 +/- 4.5%). The ex vivo susceptibility of LDL to oxidation was higher after the 1.7-g/d EPA+DHA intervention than after the control and ALA interventions (P < 0.05). There was no significant change in plasma alpha-tocopherol concentrations or in whole plasma antioxidant status in any of the groups. CONCLUSION: At estimated biologically equivalent intakes, dietary ALA and EPA+DHA have different physiologic effects.
Influence of fish oil supplementation on in vivo a...[Eur J Clin Nutr. 2003] - PubMed Result
CONCLUSION: According to our findings, fish oil supplementation leads to increased in vivo oxidation and increased in vitro oxidation susceptibility of LDL particles. More studies are needed to clarify the clinical importance of this finding.
New Questions on Treating Cholesterol - New York Times
Because the link between excessive LDL cholesterol and cardiovascular disease has been so widely accepted, the Food and Drug Administration generally has not required drug companies to prove that cholesterol medicines actually reduce heart attacks before approval.
Junkfood Science: How’d we get here? If you’re confused about the latest statin and cholesterol news, this information may help...
As the New York Times reported just this morning:

Because the link between excessive LDL cholesterol and cardiovascular disease has been so widely accepted, the Food and Drug Administration generally has not required drug companies to prove that cholesterol medicines actually reduce heart attacks before approval.

Junkfood Science: How’d we get here? If you’re confused about the latest statin and cholesterol news, this information may help...
Yes, you read that correctly. Statins (like weight loss drugs) have not had to show they actually save lives or extend lives of patients. They have been given approval based solely on false surrogate endpoints. “We’ve approved drugs because they lower LDL-cholesterol without specific evidence that they decreased the rate of heart disease,” said Dr. Robert Temple, M.D., director of the FDA’s Office of Medical Policy.
Health & Nutrition by Michael R. Eades, M.D. » Ketosis cleans our cells
Linus Pauling Institute at Oregon State University
Drug Interactions -- Gamma-linolenic acid supplements, such as evening primrose oil or borage seed oil, may increase the risk of seizures in people on phenothiazines, such as chlorpromazine (150). High doses of black currant seed oil, borage seed oil, evening primrose oil, flaxseed oil and fish oil may inhibit platelet aggregation, and should be used with caution in people on anticoagulant medications. In particular, people taking fish oil or long-chain omega-3 fatty acid (EPA and DHA) supplements in combination with anticoagulant drugs, including aspirin, clopidogrel (Plavix), dalteparin (Fragmin), dipyridamole (Persantine), enoxaparin (Lovenox), heparin, ticlopidine (Ticlid) and warfarin (Coumadin), should have their coagulation status monitored using a standardized prothrombin time assay (INR). One small study found that 3 g/day or 6 g/day of fish oil did not affect INR values in 10 patients on warfarin over a 4-week period (161). However, a recent case report described an individual who required a reduction of her warfarin dose when she doubled her fish oil dose from 1 g/day to 2 g/day (162).
Junkfood Science: Reading the evidence closely — statins for seniors
This 22% reduction in relative risk, however did not reach statistical significance.
Meta-Analysis Shows Statins Reduce All-Cause Mortality in Elderly Patients
Junkfood Science: Reading the evidence closely — statins for seniors
According to Dr. Ravnskov and colleagues:One may question whether statin treatment should be used at all because the small absolute risk reduction rewards may be outweighed by potential serious long-term side effects.
The International Network of Cholesterol Skeptics
Junkfood Science: Reading the evidence closely — statins for seniors
They compiled one of the clearest illustrations of the importance of looking at actual risks in order to gain a better understanding of what study findings mean:
Junkfood Science: Reading the evidence closely — statins for seniors
When you read statin studies, more commonly their benefits are described as reducing risks for surrogate endpoints, such as lab values, or for nonfatal cardiovascular events and unstable angina, and all-cause mortality isn’t mentioned at all.
Junkfood Science: Reading the evidence closely — statins for seniors
The endpoint that people most care about is whether the treatment actually prolongs life, which makes total mortality the most important consideration, not just heart disease mortality. The PROSPER trial found that while there were slightly fewer deaths from heart disease, there were more deaths from other causes, such as cancers and strokes. The all-cause mortality in this study differed by only 0.2% (10.3% in statin group and 10.5% in placebo control group). This is a clinically insignificant difference, and led three dozen professionals to write the National Institutes of Health to raise serious concerns about the lack of scientific evidence behind recommendations for statin use in elderly patients.
Junkfood Science: Reading the evidence closely — statins for seniors
Hypothesis: lipoprotein(a) is a surrogate for ascorbate.
Dr. Rath Research Institute
The Dr. Rath Health Foundation | Responsibility for a healthy world
Heart Disease is an early form of the sailor’s disease scurvy. In my presentation I can only focus on the most compelling evidence. For more details I encourage you to visit our research website (www.dr-rath-research.org).
The Famous Pauling/Rath Heart Disease Therapy
Foods highest in Fructose
The Famous Pauling/Rath Heart Disease Therapy
Nutrition & Metabolism | Full text | Fructose, insulin resistance, and metabolic dyslipidemia
There is an urgent need for increased public awareness of the risks associated with high fructose consumption and greater efforts should be made to curb the supplementation of packaged foods with high fructose additives. The present review will discuss the trends in fructose consumption, the metabolic consequences of increased fructose intake, and the molecular mechanisms leading to fructose-induced lipogenesis, insulin resistance and metabolic dyslipidemia.
Carbohydrate metabolism
One of the strange things here is the role of fructose. Why is fructose such a strong signal for release of glucokinase. Remember, glucokinase is "not interested" in reacting with fructose. It is specific for glucose. The enzyme required to initiate fructose metabolism, fructokinase, is only found in quantity in the liver (and sperm cells). Furthermore, it is not under metabolic control. If fructose comes to the liver, it will be taken up and very quickly metabolized!
JAMA -- High-Dose Atorvastatin vs Usual-Dose Simvastatin for Secondary Prevention After Myocardial Infarction: The IDEAL Study: A Randomized Controlled Trial, November 16, 2005, Pedersen et al. 294 (19): 2437
Conclusions In this study of patients with previous MI, intensive lowering of LDL-C did not result in a significant reduction in the primary outcome of major coronary events, but did reduce the risk of other composite secondary end points and nonfatal acute MI. There were no differences in cardiovascular or all-cause mortality. Patients with MI may benefit from intensive lowering of LDL-C without an increase in noncardiovascular mortality or other serious adverse reactions.
After Myocardial Infarction: The IDEAL Study: A Randomized Controlled Trial
The bottom line: This study indicates but does not prove that lowering cholesterol below currently established goals could have a positive effect on patients with known heart disease and at high risk of further problems.
Science Blog -- Ulcer-Causing Bacteria Also May Be Associated With Heart Disease
Low Serum Cholesterol : Hazardous to Health? -- Meilahn 92 (9): 2365 -- Circulation
Is having very low cholesterol levels hazardous to health? There is evidence to suggest that it might be. In 1990, an NIH conference concluded from a meta-analysis of 19 studies that men and, to a lesser extent, women with a total serum cholesterol level below 4.2 mmol/L (160 mg/dL) (6th percentile) exhibited about a 10% to 20% excess total mortality compared with those with a cholesterol level between 4.2 and 5.2 mmol/L (160 to 199 mg/dL).1 Specifically, excess causes of death included cancer (primarily lung and hematopoietic), respiratory and digestive disease, violent death (suicide and trauma), and hemorrhagic stroke. On the basis of this and other reports, a debate arose on whether recommendations for lowering cholesterol should be directed at the entire population or only toward those at high risk of coronary heart disease. Would shifting the entire cholesterol distribution downward subject those individuals at the low end of the scale to increased risk of noncardiovascular disease?
Le Jacq | Full-Text Article From Preventive Cardiology
Severe graft disease occurs in patients at a rate of approximately 15% within the first year of coronary artery bypass grafting (CABG). In this study, the authors examined predictors of the combined end point of death, nonfatal myocardial infarction (MI), and bypass graft disease at 2-year follow-up after CABG. One hundred twenty-one consecutive patients were included in this study after informed consent was obtained. In univariate analysis, there was a significantly (P<.05) higher homocysteine level (11.0 ng/mol vs 9.7 ng/mol, P=.04) in patients who met the combined end point vs those who did not. There were no statistically significant differences in the following: low-density lipoprotein cholesterol, high-sensitivity C-reactive protein, and lipoprotein(a) values; age; body mass index; smoking and diabetes status; statin or aspirin use; creatinine level; hematologic markers; left ventricular ejection fraction; number of bypass grafts; and distribution of coronary artery disease. Logistic regression analysis modeling for low-density lipoprotein cholesterol, lipoprotein(a), fibrinogen, and homocysteine showed that homocysteine value (P=.016) was an independent predictor of the primary combined end point.
JAMA -- Abstract: Cholesterol and mortality. 30 years of follow-up from the Framingham study, April 24, 1987, Anderson et al. 257 (16): 2176
From 1951 to 1955 serum cholesterol levels were measured in 1959 men and 2415 women aged between 31 and 65 years who were free of cardiovascular disease (CVD) and cancer. Under age 50 years, cholesterol levels are directly related with 30-year overall and CVD mortality; overall death increases 5% and CVD death 9% for each 10 mg/dL. After age 50 years there is no increased overall mortality with either high or low serum cholesterol levels. There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years (11% overall and 14% CVD death rate increase per 1 mg/dL per year drop in cholesterol levels). Under age 50 years these data suggest that having a very low cholesterol level improves longevity. After age 50 years the association of mortality with cholesterol values is confounded by people whose cholesterol levels are falling--perhaps due to diseases predisposing to death.
Total serum cholesterol levels and mortality risk ...[Arch Intern Med. 1993] - PubMed Result
CONCLUSIONS: Physicians should be cautious about initiating cholesterol-lowering treatment in men and women above 65 to 70 years of age. Only randomized clinical trials in older people can settle the debate over the efficacy and cost-effectiveness of lipid-lowering interventions for reducing mortality and morbidity in this population.
The Lancet
Findings

Mean cholesterol fell significantly with increasing age. Age-adjusted mortality rates were 68·3, 48·9, 41·1, and 43·3 for the first to fourth quartiles of cholesterol concentrations, respectively. Relative risks for mortality were 0·72 (95% CI 0·60–0·87), 0·60 (0·49–0·74), and 0·65 (0·53–0·80), in the second, third, and fourth quartiles, respectively, with quartile 1 as reference. A Cox proportional hazard model assessed changes in cholesterol concentrations between examinations three and four. Only the group with low cholesterol concentration at both examinations had a significant association with mortality (risk ratio 1·64, 95% CI 1·13–2·36). Interpretation

We have been unable to explain our results. These data cast doubt on the scientific justification for lowering cholesterol to very low concentrations (<4·65 mmol/L) in elderly people.

UdoErasmus.com > Articles by Udo Erasmus > Fats, Oils, EFA's, Nutrition, Health, Omega3, Essential Fatty Acids, etc...!!
When the body has as much DHA as it needs, feedback inhibition stops further conversion. Without this inhibition, toxicity could result from excess DHA production. Let me give an example. An analysis of fish oil studies showed that too much fish oil increases inflammation due to the extreme sensitivity of DHA to damage caused by oxidative stress4. Giving n-3 in the more stable form of ALA is safer because it gives the body better metabolic control and prevents DHA overdosing. Some prominent Canadian health researchers have stated for more than 10 years that they prefer the basic n-3 ALA to fish oils because of this better metabolic control that ALA affords the body.
Resolving the Coronary Artery Disease Epidemic through Plant-Based Nutrition
The world's advanced countries have easy access to plentiful high fat food; ironically, it is this rich diet that produces atherosclerosis. In the world's poorer nations, many people subsist on a primarily plant-based diet, which is far healthier, especially in terms of heart disease. To treat coronary heart disease, a century of scientific investigation has produced a device-driven, risk factor-oriented strategy. Nevertheless, many patients treated with this approach experience progressive disability and death. This strategy is a rear-guard defensive. In contrast, compelling data from nutritional studies, population surveys, and interventional studies supports the effectiveness of a plant-based diet and aggressive lipid-lowering to arrest, prevent, and selectively reverse heart disease. In essence, this is an offensive strategy. The single biggest step toward adopting this strategy would be to have United States dietary guidelines support a plant-based diet. An expert committee purged of industrial and political influence is required to assure that science is the basis for dietary recommendations.
McDougall Program Advanced Study Weekend
Make Yourself Heart Attack Proof
Superb talk by doctor/researcher on how plant based, low fat diet reversed heart disease. Quite inspiring stuff.

Fats and Oils: The significance of temperature - Second Opinions, UK
Have you ever wondered why polyunsaturated margarine has to be kept in a fridge, yet coconut oil can be kept out at room temperature for a year or more without any untoward effects? All fats and oils in Nature are a mixture of saturated, monounsaturated and polyunsaturated fatty acids. The only difference between them is the proportions of each. Whether they are in plant or animal tissues, this is governed by the temperature at which the different fats and oils are designed to operate. This point, which is often neglected when discussing the healthiness or otherwise of fats and oils, is actually the most important consideration. The degree of saturation or unsaturation determines not only a fat’s melting point, but also its chemical stability and its likelihood of auto-oxidising and creating harmful free radicals. The higher the proportion of saturated fatty acids a fat is, the less likely it is to go rancid; the more polyunsaturated fatty acids it contains, the more difficult it is to stop it going bad.
Effects of dietary cholesterol and fatty acids on ...[J Clin Invest. 1982] - PubMed Result
These diets, therefore, caused an increase in the number of LDL particles of virtually unchanged physical and biological properties. On the diet with low P/S ratio, HDL2 rose, whereas this effect was absent on diets with high P/S ratios. The response of LDL to dietary manipulations is consonant with epidemiologic data relating diets high in cholesterol and saturated fat to atherogenesis. The response of HDL2, however, is opposite to that of its putative role as a negative risk factor. Further work is needed to clarify this interesting paradox.
Big Fat Lies with Gary Taubes, 02/06/08 Stevens Institute of Technology
Longer talk by Taubes explaining the history of carb's role on obsesity. Excellent stuff! Well worth listening to.

Dr. Weil Endorses Gary Taubes' Good Calories, Bad Calories
Andrew Weil praises Taubes' Good Calories, Bad Calories book.

The effect of a low-fat, high-carbohydrate diet on...[Eur J Clin Nutr. 1998] - PubMed Result
CONCLUSIONS: Replacement of saturated fat with carbohydrate from grains, vegetables, legumes, and fruit reduces total and LDL cholesterol with only a minor effect on HDL cholesterol and triglyceride. It seems that when free living individuals change to a fibre rich high-carbohydrate diet appropriate food choices lead to a modest weight reduction. This may explain why the marked elevation of triglyceride and reduction of HDL cholesterol observed on strictly controlled high-carbohydrate diets may not occur when such diets are followed in practice.
The association between cheese consumption and car...[J Hum Nutr Diet. 2008] - PubMed Result
Men eating cheese looks bad, but I don't have access to the study details. Abstract is too general regarding amounts of cheese and other components of subjects' diet.
Replacement of carbohydrate by protein in a conven...[Clin Invest Med. 1999] - PubMed Result
CONCLUSIONS: Moderate replacement of dietary carbohydrate with low-fat, high-protein foods in a diet containing a conventional level of fat significantly improved plasma lipoprotein cardiovascular risk profiles in healthy normolipidemic subjects.
CNN.com - Transcripts
Gary Taube on Larry King.
JAMA -- Abstract: Effects of a Low-Glycemic Load vs Low-Fat Diet in Obese Young Adults: A Randomized Trial, May 16, 2007, Ebbeling et al. 297 (19): 2092
Results Change in body weight and body fat percentage did not differ between the diet groups overall. However, insulin concentration at 30 minutes after a dose of oral glucose was an effect modifier (group x time x insulin concentration at 30 minutes: P = .02 for body weight and P = .01 for body fat percentage). For those with insulin concentration at 30 minutes above the median (57.5 µIU/mL; n = 28), the low–glycemic load diet produced a greater decrease in weight (–5.8 vs –1.2 kg; P = .004) and body fat percentage (–2.6% vs –0.9%; P = .03) than the low-fat diet at 18 months. There were no significant differences in these end points between diet groups for those with insulin concentration at 30 minutes below the median level (n = 28). Insulin concentration at 30 minutes after a dose of oral glucose was not a significant effect modifier for cardiovascular disease risk factors. In the full cohort, plasma high-density lipoprotein cholesterol and triglyceride concentrations improved more on the low–glycemic load diet, whereas low-density lipoprotein cholesterol concentration improved more on the low-fat diet.

Conclusions Variability in dietary weight loss trials may be partially attributable to differences in hormonal response. Reducing glycemic load may be especially important to achieve weight loss among individuals with high insulin secretion. Regardless of insulin secretion, a low–glycemic load diet has beneficial effects on high-density lipoprotein cholesterol and triglyceride concentrations but not on low-density lipoprotein cholesterol concentration.

What if It's All Been a Big Fat Lie? - New York Times
The primary role of insulin is to regulate blood-sugar levels. After you eat carbohydrates, they will be broken down into their component sugar molecules and transported into the bloodstream. Your pancreas then secretes insulin, which shunts the blood sugar into muscles and the liver as fuel for the next few hours. This is why carbohydrates have a significant impact on insulin and fat does not. And because juvenile diabetes is caused by a lack of insulin, physicians believed since the 20's that the only evil with insulin is not having enough.

But insulin also regulates fat metabolism. We cannot store body fat without it. Think of insulin as a switch. When it's on, in the few hours after eating, you burn carbohydrates for energy and store excess calories as fat. When it's off, after the insulin has been depleted, you burn fat as fuel. So when insulin levels are low, you will burn your own fat, but not when they're high.

What if It's All Been a Big Fat Lie? - New York Times
The crucial example of how the low-fat recommendations were oversimplified is shown by the impact -- potentially lethal, in fact -- of low-fat diets on triglycerides, which are the component molecules of fat. By the late 60's, researchers had shown that high triglyceride levels were at least as common in heart-disease patients as high L.D.L. cholesterol, and that eating a low-fat, high-carbohydrate diet would, for many people, raise their triglyceride levels, lower their H.D.L. levels and accentuate what Gerry Reaven, an endocrinologist at Stanford University, called Syndrome X. This is a cluster of conditions that can lead to heart disease and Type 2 diabetes.
What if It's All Been a Big Fat Lie? - New York Times
Some of the best scientists disagreed with this low-fat logic, suggesting that good science was incompatible with such leaps of faith, but they were effectively ignored. Pete Ahrens, whose Rockefeller University laboratory had done the seminal research on cholesterol metabolism, testified to McGovern's committee that everyone responds differently to low-fat diets. It was not a scientific matter who might benefit and who might be harmed, he said, but a betting matter. Phil Handler, then president of the National Academy of Sciences, testified in Congress to the same effect in 1980. What right, Handler asked, has the federal government to propose that the American people conduct a vast nutritional experiment, with themselves as subjects, on the strength of so very little evidence that it will do them any good?
Low Density Lipoprotein Oxidation and Its Pathobiological Significance -- Steinberg 272 (34): 20963 -- Journal of Biological Chemistry
The basic pathobiology of experimental atherosclerosis appears to be very much the same as that of the human disease, suggesting that antioxidants should work in humans. Furthermore, epidemiologic studies have repeatedly shown a negative correlation between levels of dietary intake or plasma levels of antioxidant vitamins, on the one hand, and risk of coronary heart disease, on the other (65). On the other hand, the time scale over which lesions develop in animal models is very short (weeks or months) compared with the time scale over which human lesions evolve (decades). Also, the degree of antioxidant protection we can achieve in humans may be less than that achieved in animal studies.

Several clinical trials utilizing beta -carotene, designed primarily to test its possible efficacy in preventing cancer, have also recorded cardiovascular events (66-68). All of them have been negative with respect to effects on either cancer or cardiovascular disease. Unfortunately, it was not recognized until recently that beta -carotene is actually relatively ineffective in protecting LDL (much less effective than vitamin E). Carefully conducted trials in human subjects show that supplementation even with very large doses of beta -carotene (doses sufficient to increase the beta -carotene concentration in the LDL fraction severalfold) fails to protect the circulating LDL against oxidation ex vivo (69, 70). beta -Carotene is an effective quencher of singlet oxygen, but it is much less effective as a chain-interrupting antioxidant. To the extent that protection of circulating LDL is a rough index of efficacy, these beta -carotene trials should not be considered appropriate tests of the oxidative modification hypothesis.

Vitamin E, on the other hand, is very effective in protecting circulating LDL against oxidation ex vivo (69, 71, 72). The degree of protection is a function of the extent to which the vitamin E content of the circulating LDL is increased, and doses of 400-800 international units daily seem to be required for maximal protection. Only two clinical trials have been reported in which vitamin E supplementation has been used. In one of these the dosage (50 IU daily) was inadequate to protect circulating LDL, and the negative result is therefore not relevant (66). The other study utilized 400-800 IU of vitamin E daily in a placebo-controlled, double-blind trial in patients with established coronary heart disease (73). Those randomized to vitamin E showed 47% fewer nonfatal myocardial infarctions and cardiovascular deaths (the primary end point) than the control group, and the result was significant at the p = 0.001 level. Additional trials are in progress. Decisions about the use of antioxidants in human atherosclerosis should be deferred until additional data become available.

The Antioxidant Vitamins and Cardiovascular Disease: A Critical Review of Epidemiologic and Clinical Trial Data -- Jha et al. 123 (11): 860 -- Annals of Internal Medicine
Conclusion: The epidemiologic data suggest that antioxidant vitamins reduce cardiovascular disease, with the clearest effect for vitamin E; however, completed randomized trials do not support this finding. Much of this controversy should be resolved by the ongoing large-scale and long-term randomized trials designed specifically to evaluate effects on cardiovascular disease.
Low Density Lipoprotein Oxidation and Its Pathobiological Significance -- Steinberg 272 (34): 20963 -- Journal of Biological Chemistry
If oxidative modification of LDL plays a significant role in atherogenesis, its inhibition by an appropriate antioxidant should slow the progression of the disease. Indeed this has now been demonstrated in several different animal models (the LDL receptor-deficient rabbit, the cholesterol-fed New Zealand White rabbit, the cholesterol-fed hamster, the cholesterol-fed cynomolgus monkey, the LDL receptor-deficient mouse, and the apoprotein E-deficient mouse) and using one of several different antioxidants (probucol, butylated hydroxytoluene, diphenylphenylenediamine, and vitamin E) (see Ref. 12 for review and specific citations). A total of 23 studies has been reported of which 16 were strongly positive (more than 50% inhibition of the rate of progression), 2 were borderline, and 5 negative. An important question to be asked is whether the antioxidants exerted their inhibitory effect on lesion progression only because of their antioxidant properties or, possibly, because of additional biological properties. This is the same kind of problem that arises with the use of any inhibitor in biology. In fact the first antioxidant tested, probucol, does indeed have additional biological properties that might be relevant (48), including the ability to inhibit interleukin-1 release and to increase expression of cholesterol ester transfer protein. However, the fact that two antioxidants as structurally diverse as probucol and diphenylphenylenediamine share the ability to inhibit atherogenesis suggests that the effect is attributable primarily to their shared antioxidant properties. Further evidence that the effect depends upon antioxidant activity comes from the rough parallelism observed in some studies between the effectiveness of these compounds in protecting circulating LDL from oxidation in an ex vivo test system and their effectiveness in inhibiting atherogenesis (49). At this time there is insufficient evidence, however, to allow a confident prediction of the anti-atherosclerotic effectiveness of a compound from its antioxidant effectiveness ex vivo. It appears that some rather high threshold of antioxidant effect must be reached before any anti-atherosclerotic effect is evident (49, 50). Even a 4-fold prolongation of conjugated diene lag time (a commonly used measure of the resistance of LDL to oxidation) may still be inadequate. Yet many clinical correlations are being accepted as meaningful when the diene conjugation lag time is increased as little as 30%!
Low Density Lipoprotein Oxidation and Its Pathobiological Significance -- Steinberg 272 (34): 20963 -- Journal of Biological Chemistry
While oxidation of LDL in the artery wall has received the most attention, it seems very likely that oxidation of LDL takes place at many other sites, perhaps at all sites of inflammation. Because of increased vascular permeability at sites of inflammation, the concentration of LDL in the inflammatory fluid would be higher than it is in normal extracellular fluid. Because of the infiltration by neutrophils and monocyte/macrophages the conditions for LDL oxidation at inflammatory sites would be propitious. However, LDL oxidation at peripheral sites would not have the same significance as oxidation of LDL in the artery wall unless the LDL oxidized at peripheral sites reenters the bloodstream and is subsequently delivered to the artery. If LDL in the periphery were to undergo limited oxidation before reentering the blood it would have a prolonged half-life, as discussed above, and it could then be taken up into developing arterial lesions. Being already partially oxidized, this LDL might make an unusually large contribution to the further progression of the lesion. Immunochemical studies have provided evidence for the presence of oxidized LDL (or at least of antigens closely related to it) at sites of inflammation (47). The functional significance of this remains to be explored.
Low Density Lipoprotein Oxidation and Its Pathobiological Significance -- Steinberg 272 (34): 20963 -- Journal of Biological Chemistry
Heavily acetylated LDL and heavily oxidized LDL injected intravenously disappear from the plasma compartment with a very short half-life, only a matter of minutes in the rat or in the rabbit. This largely reflects extremely rapid uptake into hepatic Kuppfer cells and sinusoidal endothelial cells (43). These cells express the acetyl LDL receptor and probably other receptors for OxLDL and are highly efficient in sweeping it out of the plasma. Consequently one would not expect to find heavily oxidized LDL in the plasma at any significant concentration because it would have to be generated at an implausibly high rate. On the other hand, because MM-LDL is not a ligand for the scavenger receptors, it would probably have a half-life not much different from that of native LDL and could build up in the plasma compartment. Similarly, LDL in which a small percentage of lysine epsilon -amino groups have been masked (but not enough to make it a ligand for the scavenger receptors) might have a half-life even longer than that of native LDL and could, again, build up.
Low Density Lipoprotein Oxidation and Its Pathobiological Significance -- Steinberg 272 (34): 20963 -- Journal of Biological Chemistry
As mentioned above, modification of LDL by endothelial cells in vitro can be completely prevented by the addition of antioxidants such as vitamin E or butylated hydroxytoluene (9). It is almost completely inhibited also by the addition of as little as 5 or 10% fetal calf serum. How, then, can LDL undergo oxidative modification in vivo? Even in the extracellular fluid one would guess that the concentrations of antioxidants (proteins, vitamin C, uric acid, etc.) would be ample to inhibit cell-induced oxidative modification. Logic to the contrary notwithstanding, it does get oxidized. 1) The lipoprotein fraction gently extracted from atherosclerotic lesions (both rabbit and human) contains oxidized LDL, identified both by its physical properties and by its recognition by scavenger receptors (40); 2) immunohistochemistry using antibodies generated against oxidized LDL demonstrates the presence of oxidized LDL (or antigens very similar to it) in arterial lesions but not in normal artery (41); 3) both in animals and in humans autoantibodies that react with oxidized LDL have been demonstrated in the serum (41); 4) administration of antioxidants that can prevent oxidative modification of LDL slows the progression of atherosclerosis in several experimental animal models, as discussed in more detail below.
Low Density Lipoprotein Oxidation and Its Pathobiological Significance -- Steinberg 272 (34): 20963 -- Journal of Biological Chemistry
LDL particles rich in polyunsaturated fatty acids are more readily oxidized than are LDL particles enriched in saturated fatty acids or monounsaturated fatty acids (35).
Low Density Lipoprotein Oxidation and Its Pathobiological Significance -- Steinberg 272 (34): 20963 -- Journal of Biological Chemistry
An increase in plasma LDL levels leads to an increase in the adherence of circulating monocytes to arterial endothelial cells and at the same time to an increased rate of entry of LDL into the intima, resulting in a higher steady state concentration of LDL in the intima. There the LDL can undergo oxidative modification catalyzed by any of the major cell types found in arterial lesions, i.e. endothelial cells, smooth muscle cells, or macrophages. Even minimally oxidized LDL (MM-LDL) can increase adherence and penetration of monocytes, in part by stimulating release of MCP-1 from endothelial cells (17). MM-LDL can also stimulate release of MCSF, which can induce differentiation of the monocyte into a cell with the phenotypic pattern of the tissue macrophage, including an increase in expression of SRA (18). More fully oxidized LDL (OxLDL) is itself directly chemotactic for monocytes, and it is also, of course, one of the major ligands for SRA and other receptors on the arterial macrophage that contribute to foam cell formation. Soon after a lesion is initiated there is fragmentation of the internal elastic membrane and migration of smooth muscle cells from the media up into the intima. These smooth muscle cells do not normally express SRA but can be induced to do so (19). This may be the basis for the contribution that smooth muscle cells make to the foam cell population. A centrally important point is that the fatty streak lesion, while being clinically silent itself, is the precursor of the more complex lesions that cause stenosis and limited blood flow. These complex lesions ultimately represent the sites of thrombosis leading to myocardial infarction.
Antioxidant Riches Found in Unexpected Foods
he largest and most advanced analysis of the antioxidant content of common foods to date shows that disease-fighting antioxidants may be found in unexpected fruits and vegetables, such as beans, artichokes, and even the much-maligned Russet potato.

Researchers found that small red beans contain more disease-fighting antioxidants than both wild and cultivated blueberries, which have been heralded in recent years for their high antioxidant content. In fact, three of the top five antioxidant-rich foods studied were beans.

The study also shows that nuts and spices, such as ground cloves, cinnamon, and oregano, are rich in antioxidants, although they are generally consumed in much smaller amounts than fruits and vegetables.

Best Food Sources of Antioxidants
The Top 10 Antioxidant Foods
Chicago Journals - The Journal of Infectious Diseases
Accumulating evidence supports an association between Chlamydia pneumoniae infection and atherosclerosis. To determine whether there is a causal relationship, the effects of chronic infection with C. pneumoniae on the development of atherosclerosis in apolipoprotein E (apoE)–deficient mice were evaluated. Eight-week-old male apoE-deficient mice were inoculated intranasally with C. pneumoniae three times, at 8, 9, and 10 weeks of age. The combined area of atherosclerotic lesions in the lesser curvature of the aortic arch was measured en face by computer-assisted morphometry. The lesion area was 2.4-fold greater ( ) at 16 weeks of age and 1.6-fold greater ( ) at 20 weeks of age in infected mice than in control mice. There were no differences in total plasma cholesterol levels between groups. This study demonstrates that C. pneumoniae infection accelerates the progression of atherosclerosis in the aortic arch of apoE-deficient mice.
Effect of an energy-restricted, high-protein, low-...[Am J Clin Nutr. 2005] - PubMed Result
BACKGROUND: Limited evidence suggests that a higher ratio of protein to carbohydrate during weight loss has metabolic advantages. OBJECTIVE: The objective was to evaluate the effects of a diet with a high ratio of protein to carbohydrate during weight loss on body composition, cardiovascular disease risk, nutritional status, and markers of bone turnover and renal function in overweight women. DESIGN: The subjects were randomly assigned to 1 of 2 isocaloric 5600-kJ dietary interventions for 12 wk according to a parallel design: a high-protein (HP) or a high-carbohydrate (HC) diet. RESULTS: One hundred women with a mean (+/-SD) body mass index (in kg/m(2)) of 32 +/- 6 and age of 49 +/- 9 y completed the study. Weight loss was 7.3 +/- 0.3 kg with both diets. Subjects with high serum triacylglycerol (>1.5 mmol/L) lost more fat mass with the HP than with the HC diet (x +/- SEM: 6.4 +/- 0.7 and 3.4 +/- 0.7 kg, respectively; P = 0.035) and had a greater decrease in triacylglycerol concentrations with the HP (-0.59 +/- 0.19 mmol/L) than with the HC (-0.03 +/- 0.04 mmol/L) diet (P = 0.023 for diet x triacylglycerol interaction). Triacylglycerol concentrations decreased more with the HP (0.30 +/- 0.10 mmol/L) than with the HC (0.10 +/- 0.06 mmol/L) diet (P = 0.007). Fasting LDL-cholesterol, HDL-cholesterol, glucose, insulin, free fatty acid, and C-reactive protein concentrations decreased with weight loss. Serum vitamin B-12 increased 9% with the HP diet and decreased 13% with the HC diet (P < 0.0001 between diets). Folate and vitamin B-6 increased with both diets; homocysteine did not change significantly. Bone turnover markers increased 8-12% and calcium excretion decreased by 0.8 mmol/d (P < 0.01). Creatinine clearance decreased from 82 +/- 3.3 to 75 +/- 3.0 mL/min (P = 0.002). CONCLUSION: An energy-restricted, high-protein, low-fat diet provides nutritional and metabolic benefits that are equal to and sometimes greater than those observed with a high-carbohydrate diet.
Beneficial effect of low carbohydrate in low calor...[Diabetes Res Clin Pract. 2004] - PubMed Result
The adequate composition of carbohydrate and fat in low calorie diets for type 2 diabetes mellitus patients with obesity is not fully established. The aim of this study was to investigate the effects of low carbohydrate diet on glucose and lipid metabolism, especially on visceral fat accumulation, and comparing that of a high carbohydrate diet. Obese subjects with type 2 diabetes mellitus were randomly assigned to take a low calorie and low carbohydrate diet (n = 11, 1000 kcal per day, protein:carbohydrate:fat = 25:40:35) or a low calorie and high carbohydrate diet (n = 11, 1000 kcal per day, protein:carbohydrate:fat = 25:65:10) for 4 weeks. Similar decreases in body weight and serum glucose levels were observed in both groups. Fasting serum insulin levels were reduced in the low carbohydrate diet group compared to the high carbohydrate diet group (-30% versus -10%, P < 0.05). Total serum cholesterol and triglyceride levels decreased in both groups, but were not significantly different from each other. High-density lipoprotein-cholesterol (HDL-C) increased in the low carbohydrate diet group but not in the high carbohydrate diet group (+15% versus 0%, P < 0.01). There was a larger decrease in visceral fat area measured by computed tomography in the low carbohydrate diet group compared to the high carbohydrate diet group (-40 cm(2) versus -10 cm(2), P < 0.05). The ratio of visceral fat area to subcutaneous fat area did not change in the high carbohydrate diet group (from 0.70 to 0.68), but it decreased significantly in the low carbohydrate diet group (from 0.69 to 0.47, P < 0.005). These results suggest that, when restrict diet was made isocaloric, a low calorie/low carbohydrate diet might be more effective treatment for a reduction of visceral fat, improved insulin sensitivity and increased in HDL-C levels than low calorie/high carbohydrate diet in obese subjects with type 2 diabetes mellitus.
The effects of low-carbohydrate versus conventiona...[Ann Intern Med. 2004] - PubMed Result
BACKGROUND: A previous paper reported the 6-month comparison of weight loss and metabolic changes in obese adults randomly assigned to either a low-carbohydrate diet or a conventional weight loss diet. OBJECTIVE: To review the 1-year outcomes between these diets. DESIGN: Randomized trial. SETTING: Philadelphia Veterans Affairs Medical Center. PARTICIPANTS: 132 obese adults with a body mass index of 35 kg/m2 or greater; 83% had diabetes or the metabolic syndrome. INTERVENTION: Participants received counseling to either restrict carbohydrate intake to <30 g per day (low-carbohydrate diet) or to restrict caloric intake by 500 calories per day with <30% of calories from fat (conventional diet). MEASUREMENTS: Changes in weight, lipid levels, glycemic control, and insulin sensitivity. RESULTS: By 1 year, mean (+/-SD) weight change for persons on the low-carbohydrate diet was -5.1 +/- 8.7 kg compared with -3.1 +/- 8.4 kg for persons on the conventional diet. Differences between groups were not significant (-1.9 kg [95% CI, -4.9 to 1.0 kg]; P = 0.20). For persons on the low-carbohydrate diet, triglyceride levels decreased more (P = 0.044) and high-density lipoprotein cholesterol levels decreased less (P = 0.025). As seen in the small group of persons with diabetes (n = 54) and after adjustment for covariates, hemoglobin A1c levels improved more for persons on the low-carbohydrate diet. These more favorable metabolic responses to a low-carbohydrate diet remained significant after adjustment for weight loss differences. Changes in other lipids or insulin sensitivity did not differ between groups. LIMITATIONS: These findings are limited by a high dropout rate (34%) and by suboptimal dietary adherence of the enrolled persons. CONCLUSION: Participants on a low-carbohydrate diet had more favorable overall outcomes at 1 year than did those on a conventional diet. Weight loss was similar between groups, but effects on atherogenic dyslipidemia and glycemic control were still more favorable with a low-carbohydrate diet after adjustment for differences in weight loss.
A low-carbohydrate, ketogenic diet versus a low-fa...[Ann Intern Med. 2004] - PubMed Result
BACKGROUND: Low-carbohydrate diets remain popular despite a paucity of scientific evidence on their effectiveness. OBJECTIVE: To compare the effects of a low-carbohydrate, ketogenic diet program with those of a low-fat, low-cholesterol, reduced-calorie diet. DESIGN: Randomized, controlled trial. SETTING: Outpatient research clinic. PARTICIPANTS: 120 overweight, hyperlipidemic volunteers from the community. INTERVENTION: Low-carbohydrate diet (initially, <20 g of carbohydrate daily) plus nutritional supplementation, exercise recommendation, and group meetings, or low-fat diet (<30% energy from fat, <300 mg of cholesterol daily, and deficit of 500 to 1000 kcal/d) plus exercise recommendation and group meetings. MEASUREMENTS: Body weight, body composition, fasting serum lipid levels, and tolerability. RESULTS: A greater proportion of the low-carbohydrate diet group than the low-fat diet group completed the study (76% vs. 57%; P = 0.02). At 24 weeks, weight loss was greater in the low-carbohydrate diet group than in the low-fat diet group (mean change, -12.9% vs. -6.7%; P < 0.001). Patients in both groups lost substantially more fat mass (change, -9.4 kg with the low-carbohydrate diet vs. -4.8 kg with the low-fat diet) than fat-free mass (change, -3.3 kg vs. -2.4 kg, respectively). Compared with recipients of the low-fat diet, recipients of the low-carbohydrate diet had greater decreases in serum triglyceride levels (change, -0.84 mmol/L vs. -0.31 mmol/L [-74.2 mg/dL vs. -27.9 mg/dL]; P = 0.004) and greater increases in high-density lipoprotein cholesterol levels (0.14 mmol/L vs. -0.04 mmol/L [5.5 mg/dL vs. -1.6 mg/dL]; P < 0.001). Changes in low-density lipoprotein cholesterol level did not differ statistically (0.04 mmol/L [1.6 mg/dL] with the low-carbohydrate diet and -0.19 mmol/L [-7.4 mg/dL] with the low-fat diet; P = 0.2). Minor adverse effects were more frequent in the low-carbohydrate diet group. LIMITATIONS: We could not definitively distinguish effects of the low-carbohydrate diet and those of the nutritional supplements provided only to that group. In addition, participants were healthy and were followed for only 24 weeks. These factors limit the generalizability of the study results. CONCLUSIONS: Compared with a low-fat diet, a low-carbohydrate diet program had better participant retention and greater weight loss. During active weight loss, serum triglyceride levels decreased more and high-density lipoprotein cholesterol level increased more with the low-carbohydrate diet than with the low-fat diet.
A low-carbohydrate, ketogenic diet versus a low-fa...[Ann Intern Med. 2004] - PubMed Result
CONCLUSIONS: Compared with a low-fat diet, a low-carbohydrate diet program had better participant retention and greater weight loss. During active weight loss, serum triglyceride levels decreased more and high-density lipoprotein cholesterol level increased more with the low-carbohydrate diet than with the low-fat diet.
Angina pectoris and atherosclerotic risk factors i...[Am J Cardiol. 2008] - PubMed Result
Cardiovascular symptom relief is a major indicator for revascularization procedures. To examine the effects of intensive lifestyle modification on symptom relief, we investigated changes in angina pectoris, coronary risk factors, quality of life, and lifestyle behaviors in patients with stable coronary artery disease enrolled in the multisite cardiac lifestyle intervention program, an ongoing health insurance-covered lifestyle intervention conducted at 22 sites in the united states. Patients with coronary artery disease (nonsmokers; 757 men, 395 women; mean age 61 years) were asked to make changes in diet (10% calories from fat, plant based), engage in moderate exercise (3 hours/week), and practice stress management (1 hour/day). At baseline, 108 patients (43% women) reported mild angina and 174 patients (37% women) reported limiting angina. By 12 weeks, 74% of these patients were angina free, and an additional 9% moved from limiting to mild angina. This improvement in angina was significant for patients with mild and limiting angina at baseline regardless of gender (p <0.01). Significant improvements in cardiac risk factors, quality of life, and lifestyle behaviors were observed, and patients with angina who became angina free by 12 weeks showed the greatest improvements in exercise capacity, depression, and health-related quality of life (p <0.05). In conclusion, the observed improvements in angina in patients making intensive lifestyle changes could drastically reduce their need for revascularization procedures.
Effect of an energy-restricted, high-protein, low-...[Am J Clin Nutr. 2005] - PubMed Result
BACKGROUND: Limited evidence suggests that a higher ratio of protein to carbohydrate during weight loss has metabolic advantages. OBJECTIVE: The objective was to evaluate the effects of a diet with a high ratio of protein to carbohydrate during weight loss on body composition, cardiovascular disease risk, nutritional status, and markers of bone turnover and renal function in overweight women. DESIGN: The subjects were randomly assigned to 1 of 2 isocaloric 5600-kJ dietary interventions for 12 wk according to a parallel design: a high-protein (HP) or a high-carbohydrate (HC) diet. RESULTS: One hundred women with a mean (+/-SD) body mass index (in kg/m(2)) of 32 +/- 6 and age of 49 +/- 9 y completed the study. Weight loss was 7.3 +/- 0.3 kg with both diets. Subjects with high serum triacylglycerol (>1.5 mmol/L) lost more fat mass with the HP than with the HC diet (x +/- SEM: 6.4 +/- 0.7 and 3.4 +/- 0.7 kg, respectively; P = 0.035) and had a greater decrease in triacylglycerol concentrations with the HP (-0.59 +/- 0.19 mmol/L) than with the HC (-0.03 +/- 0.04 mmol/L) diet (P = 0.023 for diet x triacylglycerol interaction). Triacylglycerol concentrations decreased more with the HP (0.30 +/- 0.10 mmol/L) than with the HC (0.10 +/- 0.06 mmol/L) diet (P = 0.007). Fasting LDL-cholesterol, HDL-cholesterol, glucose, insulin, free fatty acid, and C-reactive protein concentrations decreased with weight loss. Serum vitamin B-12 increased 9% with the HP diet and decreased 13% with the HC diet (P < 0.0001 between diets). Folate and vitamin B-6 increased with both diets; homocysteine did not change significantly. Bone turnover markers increased 8-12% and calcium excretion decreased by 0.8 mmol/d (P < 0.01). Creatinine clearance decreased from 82 +/- 3.3 to 75 +/- 3.0 mL/min (P = 0.002). CONCLUSION: An energy-restricted, high-protein, low-fat diet provides nutritional and metabolic benefits that are equal to and sometimes greater than those observed with a high-carbohydrate diet.
Effects of weight loss from a very-low-carbohydrat...[Am J Clin Nutr. 2008] - PubMed Result
BACKGROUND: The effects of a very-low-carbohydrate, high-saturated-fat weight-loss diet (LC) on brachial artery flow-mediated dilatation (FMD) and markers of endothelial function are unknown. OBJECTIVE: The effect of an LC on markers of endothelial function and cardiovascular disease (CVD) risk was compared with that of an isocaloric high-carbohydrate, low-saturated-fat diet (HC). DESIGN: FMD and markers of endothelial function (n = 70) and CVD risk were measured before and after 8 wk of weight loss. Ninety-nine subjects aged 50.0 +/- 8.3 y with a body mass index (in kg/m2) of 33.7 +/- 4.1 completed the study. RESULTS: Mean (+/-SD) FMD did not change significantly (P = 0.55) with either diet. Pulse wave velocity improved with both diets (P < 0.01). Endothelial markers, E- and P selectin, intracellular and cellular-adhesion molecule-1, tissue-type plasminogen activator, and plasminogen activator inhibitor-1 decreased (P < 0.001), with no diet effect. Adiponectin did not change significantly. More weight (P = 0.05 for diet x time interaction) and more abdominal fat mass (P = 0.05 for diet x time interaction) were lost with the LC than with the HC. LDL cholesterol decreased more with the HC than with the LC (P < 0.05, time x diet), and C-reactive protein decreased more with the HC than with the LC (P < 0.05 for diet x time interaction). Homocysteine increased more with the LC (P < 0.01 for diet x time interaction). Folate decreased with the LC and increased with the HC (P < 0.05, time; P < 0.001 for diet x time interaction). CONCLUSION: An LC does not impair FMD. We observed beneficial effects of both diets on most of the CVD risk factors measured.
Replacement of carbohydrate by protein in a conven...[Clin Invest Med. 1999] - PubMed Result
CONCLUSIONS: Moderate replacement of dietary carbohydrate with low-fat, high-protein foods in a diet containing a conventional level of fat significantly improved plasma lipoprotein cardiovascular risk profiles in healthy normolipidemic subjects.
The effect of a low-fat, high-carbohydrate diet on...[Eur J Clin Nutr. 1998] - PubMed Result
CONCLUSIONS: Replacement of saturated fat with carbohydrate from grains, vegetables, legumes, and fruit reduces total and LDL cholesterol with only a minor effect on HDL cholesterol and triglyceride. It seems that when free living individuals change to a fibre rich high-carbohydrate diet appropriate food choices lead to a modest weight reduction. This may explain why the marked elevation of triglyceride and reduction of HDL cholesterol observed on strictly controlled high-carbohydrate diets may not occur when such diets are followed in practice.
Infected hearts - the role of bacteria in heart disease - Medicine Watch | Discover | Find Articles at BNET.com
How might C. pneumoniae play a role in heart disease? Jackson speculates that following an initial infection, it's picked up by macrophages in the lungs that then carry the bacteria all over the body through the blood. Ordinarily the macrophages would kill any bacterium they encountered. But C. pneumoniae is able to thwart the macrophages' digestive enzymes. When the macrophages arrive at the coronary arteries, they might settle beneath the arteries' surfaces and begin to suck in fat. No one knows why they take up fat, but the result is the formation of the bulging foam cells that make up plaque. Several lines of evidence support Jackson's scenario. For example, she has found the microbe in the aortas of mice infected through their noses.
Replacement of carbohydrate by protein in a conven...[Clin Invest Med. 1999] - PubMed Result
OBJECTIVE: To determine the effect on plasma lipid profiles of replacement of dietary carbohydrate by low-fat, high-protein foods. DESIGN: Cross-over randomized controlled trial. PARTICIPANTS: Ten healthy, normolipidemic subjects (8 women and 2 men). INTERVENTIONS: Subjects were randomly allocated to either a low-protein (12%) or high-protein (22%) weight-maintaining diet for 4 weeks and then switched to the alternate diet for 4 more weeks. The first 2 weeks of each diet served as an adjustment/washout period. Fat was maintained at 35% of energy, mean cholesterol intake at 230 mg per day and mean fibre intake at 24 g per day. Compliance was promoted by the use of written dietary protocols based on the food preferences of the subjects and weekly dietary consultation as required. OUTCOME MEASURES: Mean plasma levels of total, very-low-density-lipoprotein (VLDL), low-density-lipoprotein (LDL), and high-density-lipoprotein (HDL) cholesterol, and of total and very-low-density-lipoprotein (VLDL) triglycerides. Satiety levels were self-rated on a 10-point scale. RESULTS: Consumption of the high- versus the low-protein diet resulted in significant reductions in mean plasma levels of total cholesterol (3.8 v. 4.1 mmol/L, p < 0.05), VLDL cholesterol (0.20 v. 0.26 mmol/L, p < 0.02), LDL cholesterol (2.4 v. 2.6 mmol/L, p < 0.05), total triglycerides (0.69 v. 0.95 mmol/L, p < 0.005) and VLDL triglycerides (0.35 v. 0.57 mmol/L, p < 0.001), as well as in the ratio of total cholesterol to HDL cholesterol (3.1 v. 3.5, p < 0.01). A trend towards an increase in HDL cholesterol (1.26 v. 1.21 mmol/L, p = 0.30) was observed but was not statistically significant. Satiety levels tended to be higher among those eating the high-protein diet (6.1 v. 5.4, p = 0.073). CONCLUSIONS: Moderate replacement of dietary carbohydrate with low-fat, high-protein foods in a diet containing a conventional level of fat significantly improved plasma lipoprotein cardiovascular risk profiles in healthy normolipidemic subjects.
International Fish Oil Standards - IFOS
Chlamydia pneumoniae and Cardiovascular Disease
Chlamydia pneumoniae is a ubiquitous pathogen that causes acute respiratory disease. The spectrum of C. pneumoniae infection has been extended to atherosclerosis and its clinical manifestations. Seroepidemiologic studies have associated C. pneumoniae antibody with coronary artery disease, myocardial infarction, carotid artery disease, and cerebrovascular disease. The association of C. pneumoniae with atherosclerosis is corroborated by the presence of the organism in atherosclerotic lesions throughout the arterial tree and the near absence of the organism in healthy arterial tissue. C. pneumoniae has also been isolated from coronary and carotid atheromatous plaques. To determine whether chronic infection plays a role in initiation or progression of disease, intervention studies in humans have been initiated, and animal models of C. pneumoniae infection have been developed. This review summarizes the evidence for the association and potential role of C. pneumoniae in cardiovascular disease.
Glycemic load - Wikipedia, the free encyclopedia
Glycemic index and glycemic load for 100+ foods
Borzoi Reader | Catalog | Good Calories, Bad Calories by Gary Taubes
The 11 Critical Conclusions of Good Calories, Bad Calories:
  1. Dietary fat, whether saturated or not, does not cause heart disease.
  2. 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.
  3. 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.
  4. 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.
  5. Obesity is a disorder of excess fat accumulation, not overeating and not sedentary behavior.
  6. Consuming excess calories does not cause us to grow fatter any more than it causes a child to grow taller.
  7. Exercise does not make us lose excess fat; it makes us hungry.
  8. 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.
  9. 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.
  10. 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.
  11. The fewer carbohydrates we eat, the leaner we will be.
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Primary prevention of cardiovascular disease with ...[Lancet. 2004 Aug 21-27] - PubMed Result
BACKGROUND: Type 2 diabetes is associated with a substantially increased risk of cardiovascular disease, but the role of lipid-lowering therapy with statins for the primary prevention of cardiovascular disease in diabetes is inadequately defined. We aimed to assess the effectiveness of atorvastatin 10 mg daily for primary prevention of major cardiovascular events in patients with type 2 diabetes without high concentrations of LDL-cholesterol. METHODS: 2838 patients aged 40-75 years in 132 centres in the UK and Ireland were randomised to placebo (n=1410) or atorvastatin 10 mg daily (n=1428). Study entrants had no documented previous history of cardiovascular disease, an LDL-cholesterol concentration of 4.14 mmol/L or lower, a fasting triglyceride amount of 6.78 mmol/L or less, and at least one of the following: retinopathy, albuminuria, current smoking, or hypertension. The primary endpoint was time to first occurrence of the following: acute coronary heart disease events, coronary revascularisation, or stroke. Analysis was by intention to treat. FINDINGS: The trial was terminated 2 years earlier than expected because the prespecified early stopping rule for efficacy had been met. Median duration of follow-up was 3.9 years (IQR 3.0-4.7). 127 patients allocated placebo (2.46 per 100 person-years at risk) and 83 allocated atorvastatin (1.54 per 100 person-years at risk) had at least one major cardiovascular event (rate reduction 37% [95% CI -52 to -17], p=0.001). Treatment would be expected to prevent at least 37 major vascular events per 1000 such people treated for 4 years. Assessed separately, acute coronary heart disease events were reduced by 36% (-55 to -9), coronary revascularisations by 31% (-59 to 16), and rate of stroke by 48% (-69 to -11). Atorvastatin reduced the death rate by 27% (-48 to 1, p=0.059). No excess of adverse events was noted in the atorvastatin group. INTERPRETATION: Atorvastatin 10 mg daily is safe and efficacious in reducing the risk of first cardiovascular disease events, including stroke, in patients with type 2 diabetes without high LDL-cholesterol. No justification is available for having a particular threshold level of LDL-cholesterol as the sole arbiter of which patients with type 2 diabetes should receive statins. The debate about whether all people with this disorder warrant statin treatment should now focus on whether any patients are at sufficiently low risk for this treatment to be withheld.

Study of subjects with type-2 diabetes, no documented CHD, BUT one additional risk factor such as smoking. Very weird. Why include that? The report is often cited as proof statins helpful even if LDL not elevated, but subjects were not random. They had diabetes and one other risk factor such as smoking.
Myth: "One High-Saturated Fat Meal Can Be Bad"
Excellent explanation of flaws in this study. REALLY superb example of how data don't support the conclusions promulgated by the media of a medical study.
Dietary cholesterol provided by eggs and plasma li...[Curr Opin Clin Nutr Metab Care. 2006] - PubMed Result
SUMMARY: For these reasons, dietary recommendations aimed at restricting egg consumption should not be generalized to include all individuals. We need to acknowledge that diverse healthy populations experience no risk in developing coronary heart disease by increasing their intake of cholesterol but, in contrast, they may have multiple beneficial effects by the inclusion of eggs in their regular diet.
Glycation - Wikipedia, the free encyclopedia
Glycation is the first step in the evolution of these molecules through a complex series of very slow reactions in the body known as Amadori reactions, Schiff base reactions, and Maillard reactions; all lead to advanced glycation endproducts (AGEs). Some AGEs are benign, but others are more reactive than the sugars they are derived from, and are implicated in many age-related chronic diseases such as: type II diabetes mellitus (beta cell damage), cardiovascular diseases (the endothelium, fibrinogen, and collagen are damaged), Alzheimer's disease (amyloid proteins are side-products of the reactions progressing to AGEs), cancer (acrylamide and other side-products are released), peripheral neuropathy (the myelin is attacked), and other sensory losses such as deafness (due to demyelination) and blindness (mostly due to microvascular damage in the retina). This range of diseases is the result of the very basic level at which glycations interfere with molecular and cellular functioning throughout the body and the release of highly-oxidizing side-products such as hydrogen peroxide.
The Cholesterol Myths
The Cholesterol Myths -- A Fascinating Expose by Dr. Uffe Ravnskov, MD, PhD
For example, one of the largest and most often-cited studies of heart disease that is considered a cornerstone of the "diet-heart idea" is the Framingham study, which measured heart disease and many other factors in the 1950s.

The authors wrote in the report that when blood cholesterol decreased on its own, for every 1 mg/dL reduction of cholesterol, there was an 11 percent increase in heart disease mortality!

Yet how is this study often cited?

The Cholesterol Myths -- A Fascinating Expose by Dr. Uffe Ravnskov, MD, PhD
A risk factor, of course, simply means an association, or "correlation," between a disease and that factor. The first thing one learns in any introductory science course is that "correlation does not prove causation."

For an example, fire fighters are found more often around building burnings, but that does not mean that fire fighters set buildings on fire. Yet how quickly researchers forget.
Cholesterol-And-Health.com: Meet the Editor
Myth: "One High-Saturated Fat Meal Can Be Bad"
Drawing Conclusions: One Meal High In Saturated Fat is Not So Bad

We've been told that this study shows that when "you eat [saturated fat], inflammation and damage to the vessels happens immediately afterward." We've been told that it shows we must "aggressively reduce the amount of saturated fat consumed in the diet." We've been further told to throw out the beef, pork, lard, poultry fat, butter, milk, cheeses, coconut oil, palm oil and cocoa butter, replacing all these fats with safflower oil, sesame oil, sunflower seeds, corn and soybeans.

This is all on the basis of a study that couldn't differentiate the effect of coconut oil from the effect of random sampling error on flow-mediated dilation and showed people consuming coconut oil to have better flow-mediated dilation at all time points than people consuming safflower oil.

It is on the basis of a study that could not differentiate between the effects of saturated fats and the effects of low-vitamin E meals on the capacity of HDL to prevent inflammation in a Petri dish.

It is on the basis of a study that told us nothing about the amount of inflammation going on within the people consuming the meals, who are much more complex than globs of cells in a Petri dish.

Further research should uncover whether the effects seen in the test tube are due to vitamin E, to saturated or unsaturated fats, or to other causes entirely, and what relevance these observations in the test tube have for real, living people.

In the mean time, I'm going to continue cooking with CLA-rich clarified butter, and continue eating vitamin E-rich red palm oil and polyphenol-rich virgin coconut oil and extra virgin olive oil. I will continue to get my essential fatty acids from animal sources including butterfat, egg yolks from pasture-raised chickens, organ meats, cod liver oil, and fatty fish, so I can obtain the most benefit from the hormone precursors and structurally useful essential fatty acids while not overdosing on peroxide-promoting, free radical-generating, vitamin E-depleting polyunsaturates from vegetable oils like safflower oil.

Whoever's going to convince me to do otherwise has a bit more work to do.
Antiinflammatory Foods - Controlling Inflammation with Antiinflammatory Foods
Subendothelial accumulation of unesterified choles...[Atherosclerosis. 1985] - PubMed Result
This preliminary report describes the simplest and possibly earliest lipid-containing lesions induced in aortas of rabbits fed a cholesterol-containing diet. Subendothelial accumulation of unesterified cholesterol, detected with filipin dye, appears to precede morphologic changes in endothelium and accumulation of subendothelial lipid-containing "foam" cells. The origin of subendothelial unesterified cholesterol remains to be determined.
Thematic review series: The Immune System and Atherogenesis. Cytokine regulation of macrophage functions in atherogenesis -- Daugherty et al. 46 (9): 1812 -- Journal of Lipid Research
Macrophages are hypothesized to be attracted to the subendothelial space to remove noxious materials deposited at atherosclerosis-prone regions of arteries. The precise chemical identity of the substance that attracts macrophages has not been unequivocally defined, although many candidate molecules are components of modified lipoproteins (3, 4). However, the function of infiltrating cells becomes subverted and leads to their retention within the subendothelial space. In this region, it is proposed that macrophages modify adjacent lipoproteins while also providing major mechanisms of removal for modified materials from the extracellular environment. The combination of lipoprotein modification and uptake leads to macrophages becoming engorged with lipids and resulting in a morphology that is given the descriptive name of "foam cells." Lipid engorgement causes pronounced cellular hypertrophy, with the cell diameter being >10 times that of the originating monocyte. Probably as a result of the immense size increase, lipid-laden macrophages are chronically entrapped in the subendothelial space. Trapped macrophages can then invoke processes that perpetuate the continual recruitment of monocytes, leading to an expanded lesion volume. In addition, the subendothelial macrophages can influence the behavior of neighboring cell types within atherosclerotic lesions. This includes the well-characterized interaction of macrophages and T-lymphocytes (5). During late stages of atherosclerosis development, exposure of macrophage-rich areas of lesions provides a nidus for thrombus attachment that is thought to account for a high proportion of the catastrophic consequences of atherosclerosis. At each stage of lesion development described above, cytokine interactions with macrophages have the potential to be major determinants of the mechanism and magnitude of the response.
Low Density Lipoprotein Oxidation and Its Pathobiological Significance -- Steinberg 272 (34): 20963 -- Journal of Biological Chemistry
"An increase in plasma LDL levels leads to an increase in the adherence of circulating monocytes to arterial endothelial cells and at the same time to an increased rate of entry of LDL into the intima, resulting in a higher steady state concentration of LDL in the intima. There the LDL can undergo oxidative modification catalyzed by any of the major cell types found in arterial lesions, i.e. endothelial cells, smooth muscle cells, or macrophages."
Low Density Lipoprotein Oxidation and Its Pathobiological Significance -- Steinberg 272 (34): 20963 -- Journal of Biological Chemistry
The fact that low density lipoprotein (LDL)1 is extremely susceptible to oxidative damage has been known for some time (1, 2), but until quite recently this was primarily a nuisance for the student of lipoprotein metabolism. It now appears that oxidation of LDL plays a significant role in atherogenesis.
Thematic review series: The Immune System and Atherogenesis. Cytokine regulation of macrophage functions in atherogenesis -- Daugherty et al. 46 (9): 1812 -- Journal of Lipid Research
This review will focus on the role of cytokines in the behavior of macrophages, a prominent cell type of atherosclerotic lesions. Once these macrophages have immigrated into the vessel wall, they propagate the development of atherosclerosis by modifying lipoproteins, accumulating intracellular lipids, remodeling the extracellular environment, and promoting local coagulation. The numerous cytokines that have been detected in atherosclerosis, combined with the expression of large numbers of cytokine receptors on macrophages, are consistent with this axis being an important contributor to lesion development. Given the vast literature on cytokine-macrophage interactions, this review will be selective, with an emphasis on the major cytokines that have been detected in atherosclerotic lesions and their effects on properties that are relevant to lesion formation and maturation. There will be an emphasis on the role of cytokines in regulating lipid metabolism by macrophages.
Detection and Treatment of Vulnerable Plaques and Vulnerable Patients: Novel Approaches to Prevention of Coronary Events -- Waxman et al. 114 (22): 2390 -- Circulation
Fat Dictionary
Cardiovascular System / Blood / Physiology of Circulation
Role of fructose in glycation and cross-linking of...[Biochemistry. 1988] - PubMed Result
[Glycation?] "10 times more rapidly by fructose than by glucose. It is postulated that some of the protein cross-linking that occurs in vivo is fructose-induced."

Glycation is when glucose or fructose bind to a protein (or lipid?) molecule. The resulting molecule is likely to cause damage to epithelial lining of coronary (and other?) arteries. This leads to epithelial injuries, which lead to inflammation and the deposit of plaque in vessel wall (as part of the injury healing response).

What happens next? As part of the healing response to the epithelial injoy, a clot will form on the epithelial lining. If clot big enough, heart attack result. But I think the injuries cause by the glycation molecule are cumulative. Repeated injuries cause plaque buildup. If the plaque remains soft, it forms something like a pimple. It's when this pimple bursts through the epithelial lining into the vessel that a large clot may form and lead to heart attack.

What would cause the pimple burst? Possibly the glycation molecules as they damage the epithelial lining at just the wrong spot.

So if cholesterol is an important part of the immune response, and if reducing cholesterol reduces the immune response, and if the immune response is what leads to soft plaque buildup, then reduced cholesterol may lead to weaker immune system, and less soft plaque buildup. But again, the immune system is weakened by this low cholesterol approach, which explains my overall mortality/morbidity numbers don't improve--low cholesterol leads to less CHD, but deaths by other causes are increased.
Anthony Colpo - AnthonyColpo.com
What's Cholesterol Got to Do With It? - New York Times
"Vytorin is a combination of cholesterol-lowering drugs, one called Zetia and the other a statin called Zocor. Because the two drugs lower LDL cholesterol by different mechanisms, the makers of Vytorin (Merck and Schering-Plough) assumed that their double-barreled therapy would lower it more than either drug alone, which it did, and so do a better job of slowing the accumulation of fatty plaques in the arteries -- which it did not."
How Diabetics Can Live to be 100 Years Old
"Nature's diabetes cure -- Banaba leaf -- works at the molecular level by fine-tuning the damaged insulin receptor, the cause of insulin resistance. This benefit rests in its ability to selectively initiate a chemical reaction known as 'phosphorylation' at the receptor site. In effect, what is 'jammed,' becomes un-jammed thanks to the banaba leaf. Akin to a key being inserted into a lock, insulin is free to interact with the receptor, thereby triggering the cell to open the doors for blood sugar."
Fructose - Wikipedia, the free encyclopedia
Glycation - Wikipedia, the free encyclopedia
Avoid Heart Attack - 4 Ways to Avoid a Heart Attack
Exercise nearly as successful as drugs at lowering blood sugar
The Great Cholesterol Con
Anthony Colpo - Why the Low-Fat Diet is Stupid and Potentially Dangerous
LowCarb Portal | More Saturated Fat = Less Coronary Artery Disease!
Response to injury and atherogenesis -- Ross et al. 86 (3): 675 -- American Journal of Pathology
YouTube - Part 4: Heart Disease (BMA Leeds)
New model of heart disease that I find persuasive: Response to Injury. LDL/HDL levels aren't involved. Only issues are endothelial injury, thrombus formation, repair (endothelial progenitor cells, EPCs).

The International Network of Cholesterol Skeptics
spiked-essays | Essay | The Great Cholesterol Myth
Amazon.com: The Great Cholesterol Con: Anthony Colpo: Books
Colpo is very direct, working up finally to this Conclusion (p254): "There is every reason in the world to encourage people to exercise frequently, stop smoking, eat minimally processed foods, and find ways to get a handle on the stresses of modern life. The evidence for low-fat diets, on the other hand, is based on a mixture of erroneous assumptions, half-truths and downright lies."
The International Network of Cholesterol Skeptics
Malcolm Kendrick essays.
YouTube - Part 1: Cholesterol (BMA Leeds)

Preventive Cardiology - Stanford Preventive Cardiology Clinic, Stanford Preventive Cardiology Clinic, Individualized nutrition assessment, cholesterol, risk evaluation - Stanford Hospital & Clinics - Stanford University Medical Center
Patient Care - Stanford Prevention Research Center - Stanford University School of Medicine
The International Network of Cholesterol Skeptics
High cholesterol may protect against infections and atherosclerosis -- Ravnskov 96 (12): 927 -- QJM
"Many researchers have suggested that the blood lipids play a key role in the immune defense system. There is also a growing understanding that an inflammatory response of the arterial intima to injury is a crucial step in the genesis of atherosclerosis, and that infections may be one type of such injury. These two concepts are difficult to harmonize with the low-density-lipoprotein (LDL) receptor hypothesis, according to which high LDL cholesterol is the most important cause of atherosclerosis. However, the many observations that conflict with the LDL receptor hypothesis, may be explained by the idea that high serum cholesterol and/or high LDL is protective against infection and atherosclerosis."

The Great Cholesterol Con
by Anthony Colpo

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