Diet and Heart Disease – Good Calories Bad Calories

A few more highlighted passages for you all…

The observation that monounsaturated fats both lower LDL cholesterol and raise HDL also came with an ironic twist: the principal fat in red meat, eggs, and bacon is not saturated fat, but the very same monounsaturated fat as in olive oil.

I love eating bacon. I’m not joking when I tell people I eat a pound of bacon in one sitting.

All of this suggests that eating a porterhouse steak in lieu of bread or potatoes would actually reduce heart-disease risk, although virtually no nutritional authority will say so publicly. The same is true for lard and bacon.

I believe this, so does my doctor and my blood work.

The results of his seven trials have been consistent: the lower the fat in the diet and the higher the carbohydrates, the smaller and denser the LDL and the more likely the atherogenic pattern B appears; that is, the more carbohydrates and the less fat, the greater the risk of heart disease.

In the case of diet and heart disease, Ancel Keys’s hypothesis that cholesterol is the agent of atherosclerosis was considered the simplest possible hypothesis, because cholesterol is found in atherosclerotic plaques and because cholesterol was relatively easy to measure. But as the measurement technology became increasingly more sophisticated, every one of the complications that arose has implicated carbohydrates rather than fat as the dietary agent of heart
disease.

[asa full2]1400033462[/asa]

Challenge

This morning I jumped on the scale and it read 224.8

I’ve reached my goal. Looking in the mirror with a critical eye I feel like i can lose another 25 pounds and actually see some abs.

I posted this on Facebook this morning and my buddy Dave, also a low-carb convert, issued a challenge. So we’re in a race to lose 25 pounds and have visible abs.

I will keep all of you posted with my progress and I am inviting Dave to do the same here on the paunchiness blog.

In case anyone is wondering how I went from 285 in April to 225 today, all of the answers are contained here. Proper nutrition, rigorous exercise (HIIT) and a bit of self loathing.

I don’t like to lose a good competition so get ready.

Low-Carb Lowers Cardiovascular Risk Factors

It’s important to note that the low-fat diet was also calorie restricted to a near starvation amount of 1200-1800 calories a day while the low-fat included unrestricted calories.

Weight and Metabolic Outcomes After 2 Years on a Low-Carbohydrate Versus Low-Fat Diet

A Randomized Trial

Gary D. Foster, PhD; Holly R. Wyatt, MD; James O. Hill, PhD; Angela P. Makris, PhD, RD; Diane L. Rosenbaum, BA; Carrie Brill, BS; Richard I. Stein, PhD; B. Selma Mohammed, MD, PhD; Bernard Miller, MD; Daniel J. Rader, MD; Babette Zemel, PhD; Thomas A. Wadden, PhD; Thomas Tenhave, PhD; Craig W. Newcomb, MS; and Samuel Klein, MD

Background: Previous studies comparing low-carbohydrate and low-fat diets have not included a comprehensive behavioral treatment, resulting in suboptimal weight loss.

Objective: To evaluate the effects of 2-year treatment with a low-carbohydrate or low-fat diet, each of which was combined with a comprehensive lifestyle modification program.

Design: Randomized parallel-group trial. (ClinicalTrials.gov registration number: NCT00143936)

Setting: 3 academic medical centers.

Patients: 307 participants with a mean age of 45.5 years (SD, 9.7 years) and mean body mass index of 36.1 kg/m2 (SD, 3.5 kg/m2).

Intervention: A low-carbohydrate diet, which consisted of limited carbohydrate intake (20 g/d for 3 months) in the form of low–glycemic index vegetables with unrestricted consumption of fat and protein. After 3 months, participants in the low-carbohydrate diet group increased their carbohydrate intake (5 g/d per wk) until a stable and desired weight was achieved. A low-fat diet consisted of limited energy intake (1200 to 1800 kcal/d; ≤30% calories from fat). Both diets were combined with comprehensive behavioral treatment.

Measurements: Weight at 2 years was the primary outcome. Secondary measures included weight at 3, 6, and 12 months and serum lipid concentrations, blood pressure, urinary ketones, symptoms, bone mineral density, and body composition throughout the study.

Results: Weight loss was approximately 11 kg (11%) at 1 year and 7 kg (7%) at 2 years. There were no differences in weight, body composition, or bone mineral density between the groups at any time point. During the first 6 months, the low-carbohydrate diet group had greater reductions in diastolic blood pressure, triglyceride levels, and very-low-density lipoprotein cholesterol levels, lesser reductions in low-density lipoprotein cholesterol levels, and more adverse symptoms than did the low-fat diet group. The low-carbohydrate diet group had greater increases in high-density lipoprotein cholesterol levels at all time points, approximating a 23% increase at 2 years.

Limitation: Intensive behavioral treatment was provided, patients with dyslipidemia and diabetes were excluded, and attrition at 2 years was high.

Conclusion: Successful weight loss can be achieved with either a low-fat or low-carbohydrate diet when coupled with behavioral treatment. A low-carbohydrate diet is associated with favorable changes in cardiovascular disease risk factors at 2 years.

Saturated Fat – What if Bad Fat is Actually Good for You?

Today someone caught me eating cheese. I got a disappointed look that said “you’ve come so far, don’t screw it up now.”

So, I opened up my browser and Googled saturated fat. Here’s what Men’s Health had to say:

What if Bad Fat is Actually Good for You?

For decades, Americans have been told that saturated fat clogs arteries and causes heart disease. But there’s just one problem: No one’s ever proved it

Suppose you were forced to live on a diet of red meat and whole milk. A diet that, all told, was at least 60 percent fat — about half of it saturated. If your first thoughts are of statins and stents, you may want to consider the curious case of the Masai, a nomadic tribe in Kenya and Tanzania.

In the 1960s, a Vanderbilt University scientist named George Mann, M.D., found that Masai men consumed this very diet (supplemented with blood from the cattle they herded). Yet these nomads, who were also very lean, had some of the lowest levels of cholesterol ever measured and were virtually free of heart disease.

Scientists, confused by the finding, argued that the tribe must have certain genetic protections against developing high cholesterol. But when British researchers monitored a group of Masai men who moved to Nairobi and began consuming a more modern diet, they discovered that the men’s cholesterol subsequently skyrocketed.

Similar observations were made of the Samburu — another Kenyan tribe — as well as the Fulani of Nigeria. While the findings from these cultures seem to contradict the fact that eating saturated fat leads to heart disease, it may surprise you to know that this “fact” isn’t a fact at all. It is, more accurately, a hypothesis from the 1950s that’s never been proved.

The first scientific indictment of saturated fat came in 1953. That’s the year a physiologist named Ancel Keys, Ph.D., published a highly influential paper titled “Atherosclerosis, a Problem in Newer Public Health.” Keys wrote that while the total death rate in the United States was declining, the number of deaths due to heart disease was steadily climbing. And to explain why, he presented a comparison of fat intake and heart disease mortality in six countries: the United States, Canada, Australia, England, Italy, and Japan.

The Americans ate the most fat and had the greatest number of deaths from heart disease; the Japanese ate the least fat and had the fewest deaths from heart disease. The other countries fell neatly in between. The higher the fat intake, according to national diet surveys, the higher the rate of heart disease. And vice versa. Keys called this correlation a “remarkable relationship” and began to publicly hypothesize that consumption of fat- causes heart disease. This became known as the diet-heart hypothesis.

At the time, plenty of scientists were skeptical of Keys’s assertions. One such critic was Jacob Yerushalmy, Ph.D., founder of the biostatistics graduate program at the University of California at Berkeley. In a 1957 paper, Yerushalmy pointed out that while data from the six countries Keys examined seemed to support the diet-heart hypothesis, statistics were actually available for 22 countries. And when all 22 were analyzed, the apparent link between fat consumption and heart disease disappeared. For example, the death rate from heart disease in Finland was 24 times that of Mexico, even though fat-consumption rates in the two nations were similar.
The other salient criticism of Keys’s study was that he had observed only a correlation between two phenomena, not a clear causative link. So this left open the possibility that something else — unmeasured or unimagined — was leading to heart disease. After all, Americans did eat more fat than the Japanese, but perhaps they also consumed more sugar and white bread, and watched more television.

Despite the apparent flaws in Keys’s argument, the diet-heart hypothesis was compelling, and it was soon heavily promoted by the American Heart Association (AHA) and the media. It offered the worried public a highly educated guess as to why the country was in the midst of a heart-disease epidemic. “People should know the facts,” Keys said in a 1961 interview with Time magazine, for which he appeared on the cover. “Then if they want to eat themselves to death, let them.”

The seven-countries study, published in 1970, is considered Ancel Keys’s landmark achievement. It seemed to lend further credence to the diet-heart hypothesis. In this study, Keys reported that in the seven countries he selected — the United States, Japan, Italy, Greece, Yugoslavia, Finland, and the Netherlands — animal-fat intake was a strong predictor of heart attacks over a 5-year period. Just as important, he noted an association between total cholesterol and heart-disease mortality. This prompted him to conclude that the saturated fats in animal foods — and not other types of fat — raise cholesterol and ultimately lead to heart disease.

Naturally, proponents of the diet-heart hypothesis hailed the study as proof that eating saturated fat leads to heart attacks. But the data was far from rock solid. That’s because in three countries (Finland, Greece, and Yugoslavia), the correlation wasn’t seen. For example, eastern Finland had five times as many heart-attack fatalities and twice as much heart disease as western Finland, despite only small differences between the two regions in animal-fat intake and cholesterol levels. And while Keys provided that raw data in his report, he glossed over it as a finding. Perhaps a larger problem, though, was his assumption that saturated fat has an unhealthy effect on cholesterol levels.

Although more than a dozen types of saturated fat exist, humans predominantly consume three: stearic acid, palmitic acid, and lauric acid. This trio comprises almost 95 percent of the saturated fat in a hunk of prime rib, a slice of bacon, or a piece of chicken skin, and nearly 70 percent of that in butter and whole milk.

Today, it’s well established that stearic acid has no effect on cholesterol levels. In fact, stearic acid — which is found in high amounts in cocoa as well as animal fat –i s converted to a monounsaturated fat called oleic acid in your liver. This is the same heart-healthy fat found in olive oil. As a result, scientists generally regard this saturated fatty acid as either benign or potentially beneficial to your health.
Palmitic and lauric acid, however, are known to raise total cholesterol. But here’s what’s rarely reported: Research shows that although both of these saturated fatty acids increase LDL (“bad”) cholesterol, they raise HDL (“good”) cholesterol just as much, if not more. And this lowers your risk of heart disease. That’s because it’s commonly believed that LDL cholesterol lays down plaque on your artery walls, while HDL removes it. So increasing both actually reduces the proportion of bad cholesterol in your blood to the good kind. This may explain why numerous studies have reported that this HDL/LDL ratio is a better predictor of future heart disease than LDL alone.

All of this muddies Keys’s claim of a clear connection between saturated-fat intake, cholesterol, and heart disease. If saturated fat doesn’t raise cholesterol in such a way that it increases heart-disease risk, then according to the scientific method, the diet-heart hypothesis must be rejected. However, in 1977 it was still a promising idea.

That was the year Congress made it government policy to recommend a low-fat diet, based primarily on the opinions of health experts who supported the diet-heart hypothesis. It was a decision met with much criticism from the scientific community, including the American Medical Association. After all, officially endorsing a low-fat diet could change the eating habits of millions of Americans, and the potential effects of this strategy were widely debated and certainly unproved.

We’ve spent billions of our tax dollars trying to prove the diet-heart hypothesis. Yet study after study has failed to provide definitive evidence that saturated-fat intake leads to heart disease. The most recent example is the Women’s Health Initiative, the government’s largest and most expensive ($725 million) diet study yet. The results, published last year, show that a diet low in total fat and saturated fat had no impact in reducing heart-disease and stroke rates in some 20,000 women who had adhered to the regimen for an average of 8 years.

But this paper, like many others, plays down its own findings and instead points to four studies that, many years ago, apparently did find a link between saturated fat and heart disease. Because of this, it’s worth taking a closer look at each.

The Los Angeles VA Hospital Study (1969) This UCLA study of 850 men reported that those who replaced saturated fats with polyunsaturated fats were less likely to die of heart disease and stroke over a 5-year period than were men who didn’t alter their diets. However, more of those who changed their diets died of cancer, and the average age of death was the same in both groups. What’s more, “through an oversight,” the study authors neglected to collect crucial data on smoking habits from about 100 men. They also reported that the men successfully adhered to the diet only half the time.

The Oslo Diet-Heart Study (1970) Two hundred men followed a diet low in saturated fat for 5 years while another group ate as they pleased. The dieters had fewer heart attacks, but there was no difference in total deaths between the two groups.

The Finnish Mental Hospital Study (1979) This trial took place from 1959 to 1971 and appeared to document a reduction in heart disease in psychiatric patients following a “cholesterol-lowering” diet. But the experiment was poorly controlled: Almost half of the 700 participants joined or left the study over its 12-year duration.
The St. Thomas’ Atherosclerosis Regression Study (1992) Only 74 men completed this 3-year study conducted at St. Thomas’ Hospital, in London. It found a reduction in cardiac events among men with heart disease who adopted a low-fat diet. There’s a major caveat, though: Their prescribed diets were also low in sugar.

These four studies, even though they have serious flaws and are tiny compared with the Women’s Health Initiative, are often cited as definitive proof that saturated fats cause heart disease. Many other more recent trials cast doubt on the diet-heart hypothesis. These studies should be considered in the context of all the other research.

In 2000, a respected international group of scientists called the Cochrane Collaboration conducted a “meta-analysis” of the scientific literature on cholesterol-lowering diets. After applying rigorous selection criteria (219 trials were excluded), the group examined 27 studies involving more than 18,000 participants. Although the authors concluded that cutting back on dietary fat may help reduce heart disease, their published data actually shows that diets low in saturated fats have no significant effect on mortality, or even on deaths due to heart attacks.

“I was disappointed that we didn’t find something more definitive,” says Lee Hooper, Ph.D., who led the Cochrane review. If this exhaustive analysis didn’t provide evidence of the dangers of saturated fat, says Hooper, it was probably because the studies reviewed didn’t last long enough, or perhaps because the participants didn’t lower their saturated-fat intake enough. Of course, there is a third possibility, which Hooper doesn’t mention: The diet-heart hypothesis is incorrect.

Ronald Krauss, M.D., won’t say saturated fats are good for you. “But,” he concedes, “we don’t have convincing evidence that they’re bad, either.”

For 30 years, Dr. Krauss — an adjunct professor of nutritional sciences at the University of California at Berkeley — has been studying the effect of diet and blood lipids on cardiovascular disease. He points out that while some studies show that replacing saturated fats with unsaturated fats lowers heart-disease risk, this doesn’t mean that saturated fats lead to clogged arteries. “It may simply suggest that unsaturated fats are an even healthier option,” he says.

But there’s more to this story: In 1980, Dr. Krauss and his colleagues discovered that LDL cholesterol is far from the simple “bad” particle it’s commonly thought to be. It actually comes in a series of different sizes, known as subfractions. Some LDL subfractions are large and fluffy. Others are small and dense. This distinction is important.

A decade ago, Canadian researchers reported that men with the highest number of small, dense LDL subfractions had four times the risk of developing clogged arteries than those with the fewest. Yet they found no such association for the large, fluffy particles. These findings were confirmed in subsequent studies.

Now here’s the saturated-fat connection: Dr. Krauss found that when people replace the carbohydrates in their diet with fat–saturated or unsaturated — the number of small, dense LDL particles decreases. This leads to the highly counterintuitive notion that replacing your breakfast cereal with eggs and bacon could actually reduce your risk of heart disease.
Men, more than women, are predisposed to having small, dense LDL. However, the propensity is highly flexible and, according to Dr. Krauss, can be switched on when people eat high-carb, low-fat diets or switched off when they reduce carbs and eat diets high in fat, including the saturated variety. “There’s a subgroup of people at high risk of heart disease who may respond well to diets low in fat,” says Dr. Krauss. “But the majority of healthy people seem to derive very little benefit from these low-fat diets, in terms of heart-disease risk factors, unless they also lose weight and exercise. And if a low-fat diet is also loaded with carbs, it can actually result in adverse changes in blood lipids.”

While Dr. Krauss is much published and highly respected — he has served twice as chairman of the writing committee of the AHA’s dietary guidelines — the far-reaching implications of his work have not been generally acknowledged. “Academic scientists believe saturated fat is bad for you,” says Penny Kris-Etherton, Ph.D., a distinguished professor of nutritional studies at Penn State University, citing as evidence the “many studies” she believes show it to be true. But not everyone accepts those studies, and their proponents find it hard to be heard. Kris-Etherton acknowledges that “there’s a good deal of reluctance toward accepting evidence suggesting the contrary.”

Take, for example, a 2004 Harvard University study of older women with heart disease. Researchers found that the more saturated fat these women consumed, the less likely it was their condition would worsen. Lead study author Dariush Mozaffarian, Ph.D., an assistant professor at Harvard’s school of public health, recalls that before the paper was published in the American Journal of Clinical Nutrition, he encountered formidable politics from other journals.

“In the nutrition field, it’s very difficult to get something published that goes against  established dogma,” says Mozaffarian. “The dogma says that saturated fat is harmful, but that is not based, to me, on unequivocal evidence.” Mozaffarian says he believes it’s critical that scientists remain open minded. “Our finding was surprising to us. And when there’s a discovery that goes against what’s established, it shouldn’t be suppressed but rather disseminated and explored as much as possible.”

Perhaps the apparent bias against saturated fat is most evident in studies on low-carbohydrate diets. Many versions of this approach are controversial because they place no limitations on saturated-fat intake. As a result, supporters of the diet-heart hypothesis have argued that low-carb diets will increase the risk of heart disease. But published research doesn’t show this to be the case. When people on low-carb diets have been compared head-to-head with those on low-fat diets, the low-carb dieters typically scored significantly better on markers of heart disease, including small, dense LDL cholesterol, HDL/LDL ratio, and triglycerides, which are a measure of the amount of fat circulating in your blood.

For example, in a new 12-week study, University of Connecticut scientists placed overweight men and women on either a low-carb or low-fat diet. Those who followed the low-carb diet consumed 36 grams of saturated fat per day (22 percent of total calories), which represented more than three times the amount in the low-fat diet. Yet despite this considerably greater intake of saturated fat, the low-carb dieters reduced both their number of small, dense LDL cholesterol and their HDL/LDL ratio to a greater degree than those who ate a low-fat diet. In addition, triglycerides decreased by 51 percent in the low-carb group–compared with 19 percent in the low-fat group.
This finding is worth noting, because even though cholesterol is the most commonly cited risk factor for heart disease, triglyceride levels may be equally relevant. In a 40-year study at the University of Hawaii, scientists found that low triglyceride levels at middle age best predicted “exceptional survival” — defined as living until age 85 without suffering from a major disease.

According to lead study author Jeff Volek, Ph.D., R.D., two factors influence the amount of fat coursing through your veins. The first, of course, is the amount of fat you eat. But the more important factor is less obvious. Turns out, your body makes fat from carbohydrates. It works like this: The carbs you eat (particularly starches and sugar) are absorbed into your bloodstream as sugar. As your carb intake rises, so does your blood sugar. This causes your body to release the hormone insulin. Insulin’s job is to return your blood sugar to normal, but it also signals your body to store fat. As a result, your liver starts converting excess blood sugar to triglycerides, or fat.

All of which helps explain why the low-carb dieters in Volek’s study had a greater loss of fat in their blood. Restricting carbs keeps insulin levels low, which lowers your internal production of fat and allows more of the fat you do eat to be burned for energy.

Yet even with this emerging data and the lack of scientific support for the diet-heart hypothesis, the latest AHA dietary guidelines have reduced the recommended amount of saturated fat from 10 percent of daily calories to 7 percent or less. “The idea was to encourage people to decrease their saturated-fat intake even further, because there’s a linear relationship between saturated-fat intake and LDL cholesterol,” says Alice H. Lichtenstein, Ph.D., Sc.D., who led the AHA nutrition committee that wrote the recommendation.

What about Krauss’s findings that not all LDL is equal? Lichtenstein says that her committee didn’t address them, but that it might in the future.

It could be that it’s not bad foods that cause heart disease, it’s bad habits. After all, in Volek’s study, participants who followed the low-fat diet — which was high in carbs — also decreased their triglycerides. “The key factor is that they weren’t overeating,” says Volek. “This allowed the carbohydrates to be used for energy rather than converted to fat.” Perhaps this is the most important point of all. If you consistently consume more calories than you burn, and you gain weight, your risk of heart disease will increase — whether you favor eating saturated fats, carbs, or both.

But if you’re living a healthy lifestyle — you aren’t overweight, you don’t smoke, you exercise regularly — then the composition of your diet may matter much less. And, based on the research of Volek and Dr. Krauss, a weight-loss or maintenance diet in which some carbohydrates are replaced with fat — even if it’s saturated — will reduce markers of heart-disease risk more than if you followed a low-fat, high-carb diet.

“The message isn’t that you should gorge on butter, bacon, and cheese,” says Volek. “It’s that there’s no scientific reason that natural foods containing saturated fat can’t, or shouldn’t, be part of a healthy diet.”

For more on this topic and a guide to foods you shouldn’t fear, check out “Fat Foods You Can Eat”.

I bought a Concept2 Model D Indoor Rowing Machine

As part of my New Years resolution to get below 200 lbs I bought myself a new rowing machine.

I’ve been really lazy lately and weighed in at 280 over the holidays. I am officially recommitted to weightless and will keep you all posted with my progress.

I rowed for 20 minutes this morning and felt like I was going to die. It’s going to be a slow start but I’m sure as my lung capacity gets back to normal I’ll be able to do a full hour.

I also started low carb yesterday. Another session on the rower and I should have all of my stored glycogen depleted.

[asa full]B001A0ZT2I[/asa]

Good Fat, Bad Fat: The Facts About Omega-3

I found an interesting article on WebMD today about Fish Oil and Omega-3. I’ve been a long time reader of Mens Health Magazine and they’ve touted the merits of fish oil for a long time.

Check out the following and let me know what you think.

Think all dietary fat is the same? Guess again
By Colette Bouchez
WebMD Weight Loss Clinic-Feature

If you ask folks what food group they should avoid, most will probably answer “fats.” While it’s true that, in large amounts, some types of fat are bad for your health (not to mention your waistline), there are some we simply can’t live without.

Among them are the omega-3 fatty acids, found in foods including walnuts, some fruits and vegetables, and coldwater fish such as herring, mackerel, sturgeon, and anchovies.

“It not only plays a vital role in the health of the membrane of every cell in our body, it also helps protect us from a number of key health threats,” says Laurie Tansman, MS, RD, CDN, a nutritionist at Mount Sinai Medical Center in New York. Continue reading “Good Fat, Bad Fat: The Facts About Omega-3”

Vitamin C and Chest Pain

I found an interesting article about chest pain and Vitamin C. The theory is that heart disease is a form of mild scurvy brought on by a lack of Vitamin C or Ascorbate Acid. Humans, other primates and guinea pigs are unable to metabolize Ascorbate in their livers and thus need to take it in through diet or supplements.

Case Report: Lysine/Ascorbate-Related Amelioration of Angina Pectoris

Linus Pauling

Abstract 
It is gratifying to report the first observation of the amelioration of effort angina by the use of high-dose L-lysine and ascorbate in a man with severe coronary artery disease (CAD). This regimen was based on the hypothesis that, in thrombotic atherosclerosis, lipoprotein(a) [Lp(a)]‹ size-heterogeneous, LDL- like particles d displaying independent risk activity for CAD ‹initiates plaque formation by binding to fibrin in the damaged arterial wall. This postulated mechanism correlates with the findings that apoliprotein(a) [apo(a)] has a striking homology to plasminogen and the Lp(a) accumulates in atherosclerotic lesions in the arteries of man (Rath et al., 1989)and the hypoascorbic guinea pig (Rath and Pauling, 1990a, 1990b) and in occluded bypass venous grafts (Cushing et al., 1989). It is hoped that the remarkable outcome in this single case will motivate clinicians to examine the efficacy of lysine and ascorbate in additional cases of refractory angina. 

Coronary Heart Disease Case History 
In late April 1991, a biochemist National Science Medalist* with a familial trait of CAD told me that he experiences effort angina, in spite of medication and three coronary bypass operations. His father and a brother both died of CAD at age 62 he had his first angina attack at age 38. Now aged 71, this biochemist has fought CAD also by reducing risk factors (i.e., not smoking, exercising moderately, and diet/ weight control‹134 Ibs. at 5’5″). His first operation in 1978 (two vein grafts and one LIMA graft) precipitated a second operation (a parallel vein graft) five months later. Stripping of saphenous veins in the first operation induced massive swelling, thrombi, and infection in his leg; bilateral pulmonary emboli; and loss of patency in a vein graft. In 1987, following an attack of unstable angina, he was hospitalized for coronary angiography, adjustment of medications, and a Tl-stress test. A third operation in April 1990 followed attacks of unstable angina, a small MI, and angiography that revealed total occlusion of his right coronary artery and all bypass grafts except for a patent LIMA graft. Unfortunately, this LIMA was lacerated while freeing dense adhesions early in the third operation and required urgent heart-lung bypass cannulation and vein-patch repair; additionally, three venous grafts were made to left coronary arteries. The operation, which diminished but did not eliminate effort angina, left him with 1.8 liters of left-sided pleural effusate that was resistant to diuretics and tapping, and took 10 months to resorb. Medication with beta-receptor and calcium-channel blockers and lovastatin was reinstated; also, 325 mg of aspirin given initially was reduced to 81 mg following bilateral eye hemorrhages and adhesions that impair his peripheral vision. To this medication, he added 6 g of ascorbate (acid form), 60 mg CoQ-10; a multivitamin tablet with minerals; additional vitamins A, E and a B-complex; lecithin; and niacin, on advice of his cardiologist to try to raise his HDL level. Nevertheless, he still had to take nitroglycerin sublingually to suppress angina during a daily two mile walk and when working in his yard. This effort angina continued to worsen, imparting a feeling of impending doom that was reinforced by his cardiologist’s admonition during a check-up in March 1991 that a fifth angiographic test and a fourth bypass operation were no longer options. Also, the saphenous veins from his groin regions and legs had all been used for previous grafts. 

Effect of the Addition of Lysine 
In this predicament and with his history of restenosis, I suggested that he continue ascorbate and add 5 g of L-lysine daily (ca., six times the lysine derived from dietary protein) to try to mitigate the atherosclerotic acitivity of Lp(a). After reading the 1990 Rath and Pauling reports and their manuscript titled “Solution to the puzzle of human cardiovascular disease”, he began taking I g of lysine in early May 1991 and reached 5 g (in divided doses eight hours apart) by mid-June. In mid-July, his HDL was, as usual, a low 28 mg/dl. A low-normal 0.9 mg/dl blood creatinine indicated that lysine could be increased, if needed. He could now walk the same two miles and do yard work without angina pain and wrote, “the effect of the lysine borders on the miraculous”. By late August, he cut up a tree with a chain saw, and in early September started painting his house. By late September, possibly from over-exertion, he again began to have angina symptoms during his walks, but after stopping strenuous work and increasing lysine to 6 g [calculated to provide a peak 280,000 molar excess in the blood over his then 6 mg/dl of Lp(a) to help compensate for the relatively high dissociation constant of lysine-Lp(a)] these symptoms stopped entirely by mid-October. His blood creatinine was still a normal 1.2 mg/dl. He attributes his newfound wellbeing to the addition of lysine to his other medications and vitamins. His wife and friends comment on his renewed vigor. 

Discussion 
This severe case of restenosing CAD was a difficult challenge to try to ameliorate by the addition of lysine. While a positive effect was anticipated, lysine had not been tested for activity in inhibiting or reversing Lp(a)-laden atherosclerotic plaques in hypoascorbemic guinea pigs (Rath and Pauling, 1990b). However, it was known that Lp(a) binds to lysine-Sepharose, immobilized fibrin and fibrinogen (Harpel et al., 1989); and the epithelial-cell receptor for plasminogen ( Gonzalez-Gronow et al., 1989). This binding specificity correlates with the genetic linkage on chromosome six and striking homology of apo(a) and plasminogen‹highly conserved multiple kringle-four domains, a kringle-five domain, and a protease domain (McLean et al., 1987). Moreover, using the molecular evolutionary clock, the loss in primates of the ability to synthesize ascorbate (Zuckerkandl and Pauling, 1962; Rath and Pauling, 1990a) and acquisition of Lp(a) (Maeda et al., 1983) both appear to have occurred about 40 million years ago. These observations and the presence of Lp(a) in sclerotic arteries (Rath et al., 1989; Rath and Pauling, 1990b) and in venous grafts (Cushing et al., 1989) indicate that atherosclerosis may be initiated by excess binding of Lp(a) to fibrin in vascular wall clots, thus interfering with normal fibrinolysis by plasmin. This thrombogenic activity, which is postulated to reside in plasmin-homologous domains of Lp(a), may help to stabilize the damaged vascular wall, especially in ascorbate deficiency (Scanu, Lawn, and Berg, 1991; Rath and Pauling, 1990a). Once bound to fibrin, the LDL-like domain of Lp(a) could promote atheromas (Scanu, Lawn, and Berg, 1991). In this scenario, high-dosage lysine could inhibit or reverse plaque accretion by binding to Lp(a). Independently, lysine benefits the heart as a precursor with methionine in the synthesis of L-carnitine, the molecule that carries fat into mitochondria for the synthesis of adenosine triphosphate (ATP) bond energy needed for muscular and other cellular activities (Cederblad and Linstedt, 1976). While his intake of 60 mg of CoQ-10, also required for ATP synthesis, prior to the addition of lysine improved his sense of wellbeing, it did not suppress his angina. Ascorbate without lysine also did not ameliorate angina, but it is needed as an antioxidant to protect the vascular wall against peroxidative damage and in hydroxylation reactions both in the synthesis of carnitine and in the conversion of procollagen to collagen (hydroxylation of prolyl and Iysyl residues) (Myllyla et al., 1984) to strengthen the extracellular matrix of the wall. 
Whatever the pathomechanisms of atherosclerosis, the addition of lysine to medications and vitamins, including ascorbate, markedly suppressed angina pectoris in this intractable case of CAD. While a single case is anecdotal, it is hoped that its remarkable success will motivate clinicians to commence studies as soon as possible of the general applicability of lysine and ascorbate in relieving angina pectoris, so as to decrease greatly the amount of human suffering with less dependence on surgical intervention. 

Footnote (p. 144) *The biochemist patient made a major contribution to this report, but wishes anonymity. 

References 
1. Cederblad G and Linstedt S: Metabolism of labeled carnitine in the rat. Archives of Biochemistry and Biophysics 175:173-182, 1976. 
2. Cushing GL, Gaubatz JW, Nava ML, Burdick BJ, Bocan TMA, Guyton JR, Weilbaecher D, DeBakey ME, Lawrie GM and Morrisett JD: Quantitation and localization of lipoprotein(a) and B in coronary artery bypass vein grafts resected at re-operation. Arteriosclerosis 9:593-603, 1989. 
3. Gonzalez-Gronow M, Edelberg J M and Pizzo SV: Further characterization of the cellular plasminogen binding site: Evidence that plasminogen 2 and lipoprotein(a) compete for the same site. Biochemistry 28:2374-2377, 1989. 
4. Harpel PC, Gordon BR and Parker TS: Plasminogen catalyzes binding of lipoprotein(a) to immobilized fibrinogen and fibrin. Proc. Natl. Acad. Sci. USA 86:3847-3851, 1989. 
5. Maeda N, Bliska JB and Smithies O: Recombination and balanced chromosome polymorphism suggested by DNA sequences 5′ to the human deltaglobin gene. Proc. Natl. Acad. Sci. USA 80:5012-5016, 1983. 
6. McLean JW, Tomlinson JE, Kuang WJ et al.: cDNA sequence of human apolipoprotein(a) is homologous to plasminogen. Nature 330:132-137, 1987. 
7. Myllyla R, Majamaa K, Gunzler V, Hanuska-Abel HM and Kivirikko KI: Ascorbate is consumed stoichiometrically in the uncoupled reactions catalyzed by prolyl-4-hydroxylase and Iysyl hydroxylase. Journal of Biological Chemistry 259:5403-5405, 1984. 
8. Rath M, Niendorf A, Reblin T, Dietel M, Krebber HJ and Beisiegel U: Detection and quantification of lipoprotein(a) in the arterial wall of 107 coronary bypass patients. Arteriosclerosis 9:579-592, 1989. 
9. Rath M and Pauling L: Hypothesis: Lipoprotein(a) is a surrogate for ascorbate. Proc.. Natl. Acad. Sci. USA 87:6204-6207, 1990a. 
10. Rath M and Pauling L: Immunological evidence for the accumulation of lipoprotein(a) in the atherosclerotic lesion of the hypoascorbemic guinea pig. Proc. Natl. Acad. Sci. USA 87:9388-9390, 1990b. 
11. Scanu M, Lawn RM and Berg K: Lipoprotein(a) and atherosclerosis. Annals of Internal Medicine 115:209-218, 1991. 
12.Zuckerkandl E and Pauling L: Molecular disease, evolution, and genic heterogeneity. In: Horizons in Biochemistry, eds. Kasha M. and Pullman B. (Academic Press, New York) pp. 189-225, 196

[asa]B00008I8NJ[/asa]

[asa]B001G7QTKG[/asa]