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Post 0

Friday, February 24, 2006 - 11:16pmSanction this postReply
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Thanks Bob.

Eating "low fat" is entirely unnatural for homo sapiens. There is no such thing as an evolutionary diet that is this low (20%) in fat. 

Ed

p.s. While there is a single South American tribe (the Yanomamo) that appears to exist on this low proportion of fat, this exception (to over 200 studied indigenous societies) merely proves the rule. The human genome is not adapted to thrive on a low fat diet.


Post 1

Friday, February 24, 2006 - 11:24pmSanction this postReply
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Here you go, from perhaps the leading researcher on ancient diets. He's here to tell you what to be eatin' -- and his name (I'm not making this up!) is Eaton ...

====================
Eaton SB. The ancestral human diet: what was it and should it be a paradigm for contemporary nutrition? Proc Nutr Soc. 2006 Feb;65(1):1-6.

The best available estimates suggest that those ancestors obtained about 35% of their dietary energy from fats, 35% from carbohydrates and 30% from protein. Saturated fats contributed approximately 7.5% total energy and harmful trans-fatty acids contributed negligible amounts. Polyunsaturated fat intake was high, with n-6:n-3 approaching 2:1 (v. 10:1 today). Cholesterol consumption was substantial, perhaps 480 mg/d.

Carbohydrate came from uncultivated fruits and vegetables, approximately 50% energy intake as compared with the present level of 16% energy intake for Americans. High fruit and vegetable intake and minimal grain and dairy consumption made ancestral diets base-yielding, unlike today's acid-producing pattern. Honey comprised 2-3% energy intake as compared with the 15% added sugars contribute currently.

Fibre consumption was high, perhaps 100 g/d, but phytate content was minimal. Vitamin, mineral and (probably) phytochemical intake was typically 1.5 to eight times that of today except for that of Na, generally <1000 mg/d, i.e. much less than that of K. The field of nutrition science suffers from the absence of a unifying hypothesis on which to build a dietary strategy for prevention; there is no Kuhnian paradigm, which some researchers believe to be a prerequisite for progress in any scientific discipline.
====================

Ed


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Post 2

Friday, February 24, 2006 - 11:27pmSanction this postReply
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For anyone interested, I'm working on a weekly grocery list for gene-friendly foods. It should be done in a week or 2. Let me know if you're interested -- and I'll post it on RoRfitness.

Ed


Post 3

Saturday, February 25, 2006 - 8:30amSanction this postReply
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Ed, I'm very interested.

Post 4

Saturday, February 25, 2006 - 8:58pmSanction this postReply
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Okay Dean, just give me a week or 2 ...

Ed


Post 5

Monday, February 27, 2006 - 1:12amSanction this postReply
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Permit me to offer a dissenting voice here. I have been on the Pritikin diet for the last 20 years, and it has lowered my blood pressure and reduced my cholesterol dramatically. Prior to going on the diet, my total cholesterol was 185. In a little over a month, it had dropped to 115. It has since gone up some, but still remains around 150. My blood pressure was 134/90 before starting the diet. In two years, it had dropped to 100/70. Right now, it averages around 110/65. I currently weigh less than I have at any time in my adult life. My doctor says that I'm in excellent health.

Nathan Pritikin, founder of the diet, had severe heart disease before he developed it, as well as a serious form of leukemia. In two years, his cardiovascular health had improved so much that his doctor, who had said that his heart disease was incurable, was stunned, and could offer no explanation. This was before the effects of serum cholesterol on cardiovascular disease were well known. Pritikin was largely responsible for making that information available to the general public and to the medical profession as well. His leukemia also went into remission shortly after he had been on the diet, and it stayed in remission for the next 25 years until he had a relapse at around the age of 70, due to a decline in immune function secondary to aging. We know now that an extremely low fat, low sugar diet can prevent cancer and in some cases reverse it, just as it can for atherosclerosis.

The Women's Health Initiative trial did not prove much of anything when it concluded that a low-fat diet doesn't reduce heart disease. The diet simply wasn't low enough in fat. This allegedly "low-fat" regimen was 29% of total calories as fat, which is far too high an amount for producing any measurable change in cardiovascular risk factors. Dean Ornish pointed this out in his criticism of the study. To get any measurable effect, you have to drop the fat content down to 10% of total calories. This has been known for some time, which means that the people conducting the study were ill informed and irresponsible in the way they designed and controlled it.

Also, Anthony's Colpo's observation that among the 3.4 percent of trial participants with pre-existing cardiovascular disease, those randomized to the low-fat diet experienced a 26% increase in the relative risk of non-fatal and fatal CHD doesn't prove much of anything, because these individuals could have had a defect in their cholesterol metabolism to begin with, which would have caused their risk factors to increase regardless of any change in diet. 3.4% is such a small portion of the trial participants as to be statistically insignificant. It is reasonable to conclude that it wasn't the low-fat diet that caused them to get worse, but that they got worse in spite of it. This happens with a very small percentage of the population that is born with very few cholesterol receptors in their livers, so that diet doesn't help them. Drugs are required, and even they are often ineffective. But these are genetic abnormalities; they are not typical of the general population.

Colpo also mentions another study in which women were given diets with different levels of saturated fat, and the ones given less saturated fat had a greater narrowing of the coronary arteries. There was no mention of whether or not total fat was reduced, and it probably was not, because the study apparently examined only the effects of saturated fat, so it would presumably have kept the total fat intake the same, in order not to confuse the results with a reduction in total fat. Yet, Colpo writes as if total fat were decreased, which is misleading, if the reduction in saturated fat was compensated for by an increase in polyunsaturated fat. It would make sense that an increase in polyunsaturated fat in place of saturated fat might be expected to increase atherosclerosis, given the greater tendency for oxidation of existing serum cholesterol from the polyunsaturated oils. Pritikin recommends keeping all fats low, including polyunsaturated fat. He also recommends keeping simple sugars low, which can raise triglycerides and increase atherosclerotic progression in susceptible individuals -- those who are hyperglycemic and hyperinsulinemic.

Colpo's own case is interesting. I'm not sure what to make of it, but it is contrary to all the research currently available on the effects of a very low-fat diet, which are positive in the vast majority of the people who try it and manage to stay on it. His experience must be kept in perspective as strictly anecdotal, although it is certainly something that should be looked into. I would want to know if he was doing anything else, like drinking alcohol, that he neglected to mention. Anecdotal cases are problematic for precisely this reason; they do not constitute large, well-controlled studies. Someone's personal report on what he did is notoriously unreliable, which is why double-blind studies are considered so important.

Personally, I think that Anthony Colpo is serving up a high-fat stew of half-truths, dietary polemics and misleading generalizations. I can cite references from the American Journal of Clinical Nutrition that contradict his assertions, especially his claim that without dietary fat, carotenes cannot be properly absorbed. Also, his claim that athletes only do well on the Pritikin diet during three or four days of a carbo-loading phase is contradicted by the evidence. Many top athletes have been on the Pritikin diet for years, and it shows dramatically in their superior performances.

The Hawaii Ironman Triathlon is a grueling annual event consisting of a 2.4-mile ocean swim, 112-mile bicycle race, and a 26.2-mile marathon run. For six weeks prior to the 1982 Ironman, Dave Scott, Scott Tinley, and Scott Molina were monitored as they trained on the Pritikin diet. In Hawaii, a special Pritikin kitchen was set up for their meals. On the day of the '82 Hawaii Triathlon, the heat was almost unbearable and the black asphalt road reached temperatures up to 115 degrees F. These three runners finished 1st, 2nd and 4th place. Dave Scott, the winner, won in a record time that was 16 minutes faster than his previous best. As it turned out, he had been following his own version of the Pritikin diet for several years and preparing his own food. One of the reasons that these athletes did so well on that diet is not only the extra glycogen from their high carb diets, but also the very low fat content of the diet, which improves circulation dramatically, as fat causes the red corpuscles and other blood cells to stick together, impairing oxygen delivery to the muscles. One runner I recommended the diet to told me how much easier it was for him to breath when he was on it.

There are many other examples of world-class athletes who owe their success to the Pritikin diet. I won't bother to list them all, but Rob de Castella is another one, who won the 1983 Rotterdam, Holland marathon in 2:08:18 (a spectacular time) and attributes his success to the Pritikin diet.

The epidemiologic evidence contradicts Colpo as well. Primitive people like the Tarahumara Indians of the Creel area of Chihuahua, Mexico follow a diet that is between 9 and 12% of total calories as fat. Their diet consists largely of corn, pinto beans, and other plant foods. They exceed the Food and Agriculture Organization/World Health Organization recommendations for vitamin A by 2 1/2 times, and only 3% of the vitamin A in their diet comes from animal products. Corn provides 56% of the vitamin A intake, and 35% comes from greens. Their adult cholesterol levels range between 100 and 140 mg/dL, and there isn't a documented case of heart disease among the entire population.

The natives of Papua, New Guinea follow a diet that has only 3% of total calories as fat, and consume only 0.7% of total calories as essential fatty acids, yet they exhibit no evidence of an essential fatty acid deficiency, which includes scaly skin, unusual pigmentation, and inability of the skin to heal. Hair loss, one of the first symptoms of an EFA deficiency, was not observed. It is believed that the ratio of linoleic acid to linolenic acid is more important than the absolute amounts. Needless to say, there is no heart disease among the New Guineans.

African tribes who are predominantly vegetarian and follow a very low-fat diet are another example. They have average serum cholesterols of 110 mg/dL and no heart disease. Wherever you look in a study of populations, those that are on something like the Pritikin diet are completely free of heart disease.

It is true that a very low-fat diet reduces testosterone; it reduces estrogen as well. All hormones are lower on the Pritikin diet, and accordingly, hormone dependent cancers, like breast and prostate. Is that such a bad thing? Colpo writes as if the more testosterone, the better.

There's a lot of angry polemics and considerable hyperbole in his article, which should lead one to be a bit skeptical of his objectivity. He is clearly rebelling against a diet that he feels did him wrong, and looking for as much intellectual ammunition to discredit it as he can. In the process, however, he ignores vast amounts of evidence, both clinical and epidemiological, that high-fat, high-cholesterol diets are atherogenic and mutagenic. If he is going to convince the medical profession that a high intake of dietary fat is nothing to worry about, he has his work cut out for him.

Also, the idea that early man followed a certain diet does not automatically mean that that diet is necessarily ideal or one that will promote optimum health. Early man had only to live long enough to reproduce and in many cases didn't live much beyond that, given the hostile conditions that he had to deal with. We have absolutely no evidence that the diet he followed would enable us to live to a ripe old age by modern standards, since our early ancestors didn't come close to living that long. In fact, much of the current evidence indicates that longevity is increased by a low-calorie diet. Gerontologist Roy Walford, who did a lot of research on the effects of diet on maximum lifespan, said that something like the Pritikin diet has been shown to enhance longevity in all animals so far studied, including primates. There is no reason to believe that human beings are any different in this respect.

Anyway, as you can see, I'm not impressed by Colpo's acerbic criticism or by his objectivity.

- Bill

Post 6

Monday, February 27, 2006 - 10:36pmSanction this postReply
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Bill, I've marshalled peer-reviewed counter-evidence to the jist of your Post #5 here ...

http://rebirthofreason.com/Forum/RoRFitness/0023.shtml

It provides peer-reviewed evidence for an increase in the top 3 killers -- cancer, cardiovascular disease, and diabetes -- from "low-fat (high-carb)" dieting.

Ed

(Edited by Ed Thompson on 2/27, 10:37pm)


Post 7

Tuesday, February 28, 2006 - 8:46pmSanction this postReply
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Bill, one of your concerns dealt with a 2004 AJCN study on angiography-confirmed atherosclerotic progression. Here's the left-out data you had argued over.

===============
Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. Am J Clin Nutr. 2004 Nov;80(5):1175-84.
 
In multivariate analyses, a higher saturated fat intake was associated with a smaller decline in mean minimal coronary diameter (P = 0.001) and less progression of coronary stenosis (P = 0.002) during follow-up. Compared with a 0.22-mm decline in the lowest quartile of intake, there was a 0.10-mm decline in the second quartile (P = 0.002), a 0.07-mm decline in the third quartile (P = 0.002), and no decline in the fourth quartile (P < 0.001); P for trend = 0.001.

This inverse association was more pronounced among women with lower monounsaturated fat (P for interaction = 0.04) and higher carbohydrate (P for interaction = 0.004) intakes and possibly lower total fat intake (P for interaction = 0.09).

Carbohydrate intake was positively associated with atherosclerotic progression (P = 0.001), particularly when the glycemic index was high.

Polyunsaturated fat intake was positively associated with progression when replacing other fats (P = 0.04) but not when replacing carbohydrate or protein. Monounsaturated and total fat intakes were not associated with progression.
===============

This study used multivariate analyses (analyses that sterilize biases) so, your initial -- and very reasonable, mind you -- criticism of this study -- doesn't hold-up under a closer scrutiny.

One interesting thing that I keep seeing in research, is that carbs kill women. Men can often be healthy on high-carbs, but women can't (not "often" anyway). Another type of individual that carbs'll kill, is the smoker.

A differential hormonal response profile in females helps explain the differential outcome -- their androgens go up on low-fat (high-carb) diets. They often get polycystic ovary syndrome on high-carb diets, too -- likely linked to the excess androgens (or excess estrogen, a natural androgen metabolite).

Don't know why high-carb diets kill smokers, though.

Overall, a good rule of thumb is to look to 2 blood lipid values: HDLs and Triglycerides. If your HDLs are low, and your TGs are high -- then carbs'll kill you.

Ed


Post 8

Wednesday, March 1, 2006 - 6:43amSanction this postReply
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Hi guys:

I am impressed with the detailed knowledge you guys seem to have about health and nutrition. I am not nearly so well-versed, but I have a lifetime's experience at trying to deal with the effects of my diet and lifestyle.

I am a little unclear what is meant by "low fat" diets... does that necessarily imply "high carb" diet? In 1998 I needed to reduce my body fat to an extreme level (for a woman - 10%) for a breast reduction surgery - apparently the very low level of body fat increases healing as well as the ultimate result. I was living in Chapel Hill, NC at the time and I used the Rice Diet program (which is popular around there as it is housed in Durham, at Duke) and spent about a year on this diet, which is very low calorie, low sodium, and low fat. It is primarily plant based, and I thought it was both low fat and low carb. Not only did my weight decrease dramatically, I felt great and my health was probably the best it has ever been. I do remember lots of lectures about what typical people consider to be a "normal" weight, "normal" level of body fat, "normal" level of fat calories consumed, etc. and how they do not result in optimal health.

Ultimately, my surgery went very well so I would call the project a success. In the past ten years, I have *not* maintained a plant based diet nor my weight loss. Drinking alcohol seems to be the sticking point for me... even the diet changes I am willing to make do not keep me at a thin body weight because I drink frequently... apparently alcohol affects the metabolism of food and nutrients in a different way than just the calorie/fat content would suggest. I think I value the social aspects of having drinks more than being at my optimal level of fitness, so I am not really sure what is the best eating plan for me.



Post 9

Wednesday, March 1, 2006 - 11:15amSanction this postReply
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Hey Ashley.

Wow, 10% IS LOW for females. I'll bet you were sportin' a 6-pack then, huh?! But, before I'd prepare to sign-off on what diet is right for you, I'd like to know 4 things:

-Your current (broad) dietary pattern -- just think of a usual plate, and of what portion of your plate that is usually covered by veggies, by meat, by starch, etc (and think of a glass, and of what portion of that glass is filled with milk, with juice, with beer, etc)

... plus, your current ...

-HDL
-total cholesterol
-triglycerides

After knowing these 4 things, I could tell you a little about which dietary patterns you'd thrive on (as well as those patterns leading to premature death & disability).

Ed


Post 10

Wednesday, March 1, 2006 - 11:57amSanction this postReply
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Currently, my eating plan (and reality) is this:

Daily -
3 servings protein (4-7 oz. depending on the protein)
3 servings fruit
5 servings vegetables (non-starch)
2-3 servings high quality starch
1 serving dairy
1 serving added fat (I don't cook with it usually, I put it on top and try to use flaxseed, hemp seed, olive or grapeseed oil. I try to make sure any meats I eat are lean cuts with no visible fat)

Weekly -
Breakfast:
Cereal + milk 3 times per week
Fruit Smoothie 2 times per week
Eggs and bagel 2 times per week

Lunch:
I eat a Lean Cuisine type meal almost every day, but some days eat yogurt and cottage cheese and/or a piece of fruit (if it wasn't a smoothie breakfast)

Dinner:
Chicken, Pork, Beef one time each per week
Fish two times per week
Green Salad with beans, chicken or seafood two times per week

I don't eat rice, pasta, or potatoes very often, although I love them
I eat two brightly colored vegetables with each dinner, I actually eat asparagus at almost every meal, often a salad, often squashes, and corn in the summer (my one starchy splurge)
I should eat more variety of greens, but I just don't like most of them.

I try to limit cheeses, chocolate, and sweets to a very small serving once or twice a week. I love these things but can't eat much of them, so I try to get very high quality specimens and enjoy them all alone as a big event.

If I snack, I try to eat popcorn, extra fruit (usually grapes), or drink very cold Crystal Lite. I drink about 100oz. of water each day.

I have one cup of coffee with cream and sugar about 3 times per week, less when it's warm out.

All that said, I also have my moments, usually alcohol and friends are involved, where I eat enormous amounts of food like pizza, nachos, chinese food, etc. Probably not more than once a month. On a day to day basis I almost never eat fast food or drink soda, and don't eat at franchise restaurants after 4pm at all.

I do drink alcohol 4 or 5 times per week. I sometimes drink my way through most of the afternoon and evening. I might have a bottle of wine/champagne (1-2 times per week), 3-4 shots of Jameson and 5-6 Yuengling Lagers (2-3 times per week), or a couple of mixed drinks (not that often).
I think this part of my diet is the most troubling health and weight wise. Like I said though, I enjoy it and don't really want to change it.

I also smoke weed most days, typically later in the night before bed. Although I don't think this affects the way I eat at all (contrary to popular belief) I do think it might affect my will to exercise and I wonder if it affects my metabolism or ability to use nutrients at all (I have no idea, just wonder).

As of 1/18/2006:
Cholesterol- 166
HDL- 34.0
LDL- 113
Triglycerides- 97

I don't exercise really. I do yoga one or two times per week. I take my dog for leisurely walks. This is probably the other part of my problem.



Post 11

Wednesday, March 1, 2006 - 8:06pmSanction this postReply
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Daaaaaaaaaaaaaaaaaaaaaang, Ashley -- you eat C-L-E-A-N! Wow. Holy smokes. Wow.

Well, anyway, it looks like (by conventional med standards) you've got some pretty good numbers here ... except that that HDL is a little on the low side -- do you know what I mean?  Here's one bad thing associated with that ...

================
Low HDL cholesterol is associated with suicide attempt among young healthy women: the Third National Health and Nutrition Examination Survey. J Affect Disord. 2005 Dec;89(1-3):25-33. Epub 2005 Nov 2.
 
RESULTS: Independent of socio-demographic variables, health risks and nutrition status, and a history of medical and psychiatric illness (including depression), a significant association between low HDL-C (< or = 40 mg/dl) and increased prevalence of suicide attempts was observed in women (OR=2.93, 95% CI=1.07-8.00). No significant evidence was found to support an association between cholesterol and suicide ideation in women. Serum cholesterol was unrelated with either suicide ideation or attempts in men. LIMITATION: The inherent limitation of cross-sectional design prevented the authors from investigating causality.
================


... and here's another ...

================
High-density lipoprotein as a therapeutic target: clinical evidence and treatment strategies. Am J Cardiol. 2005 Nov 7;96(9A):50K-58K; discussion 34K-35K. Epub 2005 Sep 15.

In prospective epidemiologic studies, every 1-mg/dL increase in HDL is associated with a 2% to 3% decrease in coronary artery disease risk, independent of low-density lipoprotein (LDL) cholesterol and triglyceride (TG) levels. The primary mechanism for this protective effect is believed to be reverse cholesterol transport, but several other anti-inflammatory, antithrombotic, and antiproliferative functions for HDL have also been identified. In recognition of these antiatherogenic effects, recent guidelines have increased the threshold for defining low levels of HDL for both men and women. The first step in achieving these revised targets is therapeutic lifestyle changes. When these measures are inadequate, pharmacotherapy specific to the patient's lipid profile should be instituted. Niacin therapy, currently the most effective means for raising HDL levels, should be initiated in patients with isolated low HDL (HDL <40 mg/dL, LDL and non-HDL at or below National Cholesterol Education Program (NCEP) targets based on global cardiovascular risk evaluation).
================

... but don't run out to chomp on niacin pills -- effective doses of niacin can damage your liver (blood tests for liver enzymes track this). I suggest (if you were to try niacin to raise your low HDLs) that you work with a healthcare professional. Other, less-risky things that have boosted HDLs before are ...

-2 to 4 hours per week of exercise
-1000mg per day of vitamin C
-4000mg per day of EPA/DHA (the omega-3 fatty acids in fish oil)
-moderate alcohol consumption
-reducing/eliminating smoking
-reducing carbohydrate intake somewhat -- while simultaneously increasing intake of saturated fat somewhat

Here's a review on this last (counter-intuitive) point ...

================
Randomized clinical trials on the effects of dietary fat and carbohydrate on plasma lipoproteins and cardiovascular disease. Am J Med. 2002 Dec 30;113 Suppl 9B:13S-24S.
 
When saturated or trans unsaturated fats are replaced with monounsaturated or n-6 polyunsaturated fats from vegetable oils, primarily low-density lipoprotein (LDL) cholesterol decreases. The LDL to high-density lipoprotein (HDL) cholesterol ratio decreases. When carbohydrates are used to replace saturated fats, in a low-fat diet, LDL and HDL decrease similarly, and the ratio is not improved; triglycerides increase as well when carbohydrate increases, except when low glycemic index foods are used.
================

Ed


Post 12

Wednesday, March 1, 2006 - 10:28pmSanction this postReply
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Ashley,

Low HDL levels in females are associated with particularly bleak outcomes. Here is some more evidence -- evidence that might get you just a little more interested in my "HDL-boosters" list above ...

================
Dyslipidemia, gender, and the role of high-density lipoprotein cholesterol: implications for therapy. Am J Cardiol. 2000 Dec 21;86(12A):15L-18L.
 
Cardiovascular disease, which kills more US women than all cancers combined, may pose an even greater risk for women than for men. For example, the risk factors, testing modalities, presenting symptoms and the therapeutic choices made for women with coronary artery disease are significantly different from those for men.

Low levels of high-density lipoprotein cholesterol (HDL-C), <35 mg/dL in men and <45 mg/dL in women, is associated with a greater risk of coronary artery disease and more progression of angiographically demonstrated disease in women, while increasing HDL-C has a more cardioprotective effect in the female than in the male population.

The total cholesterol-to-HDL-C ratio is also more predictive of coronary artery disease in women than in men. Because average HDL-C levels in women are approximately 10 mg/dL higher than in men, target HDL-C should be higher (>45 mg/dL) in women. This is not yet reflected in clinical guidelines.

Diabetes is particularly hazardous in women, and low HDL-C levels constitute a disproportionate risk for coronary artery disease in diabetic women compared with diabetic men.
================

Ed


Post 13

Thursday, March 2, 2006 - 12:56amSanction this postReply
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Bill,

One of your criticisms is the chicken-egg conundrum of whether diet causes low HDL (or sex hormones), or whether cancers causes low HDL (or sesx hormones?). What about skipping HDL (or sex hormones?), and going straight to diet-causing-cancer? ...

==================
Several recent epidemiological studies have shown an increase in breast cancer risk among women who have elevated plasma levels of testosterone, reduced levels of sex hormone-binding globulin (SHBG), and hence elevated levels of bioavailable androgens and estrogens not bound to SHBG. This endocrine profile is generally associated with obesity and chronic hyperinsulinemia, of which it is most likely a result. Lack of physical activity, obesity, and a diet rich in rapidly digestible carbohydrates and poor in fibre favour the development of insulin resistance and hyperinsulinemia.

Hyperinsulinemia and an increased IGF-I bioactivity could thus be an important physiological link between a western lifestyle, overnutrition, a hyperandrogenic sex steroid profile, and increased breast cancer risk.
==================

And what is the dietary pattern that results in chronic hyperinsulinemia? Answer: High-carb dieting (or a medium-high-carb diet alongside of a high trans, or saturated, fat intake).

Ed
[diets affect outcomes, not just markers/intermediaries of outcomes)


Post 14

Thursday, March 2, 2006 - 6:35amSanction this postReply
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Wow, Ed! Thanks for the HDL info. Here is the extent of my knowledge of cholesterol: HDL = High Density = Happy Density. LDL = Low Density = Lethal Density. That's the only way I can remember which is good and which isn't. So I need higher numbers of Happy Cholesterol? It looks like it from all those articles you referenced, I was particularly interested in the SUICIDE link. That seems like a worst possible outcome!

I was checking out your list of HDL raising ideas.

-2 to 4 hours per week of exercise

I already know I need to be making this lifestyle change. Do you know if it needs to be high intensity effort, or just moving around? I keep reading that there is a different recommendation for improved cardio health vs. burning fat or something like that.

-1000mg per day of vitamin C
-4000mg per day of EPA/DHA (the omega-3 fatty acids in fish oil)

Does this work fine if you are getting it through supplements rather than diet? If so, this seems easy enough.

-moderate alcohol consumption

Does this mean moderate consumption is improving my HDL, or that I might consider drinking more moderately so that it can improve? Seriously :-) Although I'm probably not going to modify this much.

-reducing/eliminating smoking

On Feb. 2, I decided to reduce my smoking. I was smoking about a pack a day and now I am smoking less than 10 per day. I am smoking far less than before, sometimes only a couple in a whole day if I don't go out.

-reducing carbohydrate intake somewhat -- while simultaneously increasing intake of saturated fat somewhat

I think I might be eating as little in the carb department as I am willing to go. I am not sure what increasing saturated fat means? Could I eat more meat? And if I am not reducing carbs, maybe it's a moot point.

So, right now I can start using Vitamin C and EPA/DHA supplements, and I need to start exercising more (which I already knew). I will keep trying to reduce my smoking. I have been trying to drink more wine and less beer. Do I just want my HDL to be above 40, or is there a magic target number?

Ed, thanks a lot for this info. You should charge people for it.


Post 15

Thursday, March 2, 2006 - 10:26amSanction this postReply
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If ye can manage a half hour walk every other day, or better, every day, then ye be doing ok in the exercising - for now.......

Post 16

Thursday, March 2, 2006 - 8:24pmSanction this postReply
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Hey Ashley,

Regarding aerobic exercise intensity (and using the treadmill mode), some evidence suggests you'll need to hold at least 4mph for 30 minutes 4-7 times per week (7-14 miles per week).

If -- while at 4mph -- you check your heart rate, and you find it goes above 80% of your age-predicted maximum heart rate (220-age), it would be more conservative for you to slow down (initially), and work up to the 4mph -- increasing speed 5-10% per week each week.

If you jog outside, then keep yourself in the range from 70% - 80% of maximum heart rate.


============
I keep reading that there is a different recommendation for improved cardio health vs. burning fat or something like that.
============

This is mostly a floating misconception (resting on a conceptual mistake).


============
-1000mg per day of vitamin C
-4000mg per day of EPA/DHA (the omega-3 fatty acids in fish oil)

Does this work fine if you are getting it through supplements rather than diet? If so, this seems easy enough.
============

These were "proven" to work in the supplemental form (rather than through diet). Also, I invite you to consider a more conservative dose of fish oil -- providing at least 1.5-3.0 grams of EPA+DHA. Besides, 4 grams per day is twice as expensive as 2 grams -- but not twice as effective.

Regarding alcohol, the HDL boost comes with 1-2 drinks a day.


============
Could I eat more meat? And if I am not reducing carbs, maybe it's a moot point.
============

Evidence-supported stop points (where it wouldn't be prudent to add meat -- not without also reducing carbs) would be if your LDL cholesterol were over 130, or your triglycerides were over 150. Added fish oil (along with ample water and plant-food intake), would change everything here (would take the previously-conjectured "risk" out of meat-eating).


============
Do I just want my HDL to be above 40, or is there a magic target number?
============

Above 45 is good, above 60 is great.


============
Ed, thanks a lot for this info. You should charge people for it.
============

You're welcome, Ashley.

Taking money for nutrition guidance is risky in the socialist/fascist state that I live in (Minnesota). One lady from St. Paul was arrested for this a few years back (FDA sting operation). This year, an M.D. had his license stripped -- for alternative cancer treatments.

Minnesota has the Mayo Clinic and the U of MN med school. These 2 powerhouses likely influence the level of guild socialism that is imposed by brute force here. If you don't get the official R.D. "stamp of approval" -- but you still sell guidance anyway -- then you're asking for it.

On this note, Codex Alimentarius is the new "world-wide guild socialism" act -- for nutrition and health care. Some of our Congress supports it, some don't.

Ed

(Edited by Ed Thompson on 3/02, 8:25pm)


Post 17

Friday, March 3, 2006 - 1:29pmSanction this postReply
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Ashley, I forgot 3 other things that raise HDLs:

The nutrients ...

-chromium (picolinate or polynicotinate): 400mcg (cheap, too!)
-vitamin E (mixed tocopherols): 400 IU


... and the metabolism-modifying phytochemical ...

-hydroxycitric acid (from the fruit, Garcinia cambogia): 3000mg per day (expensive)

Ed


Post 18

Friday, March 3, 2006 - 4:37pmSanction this postReply
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Ed, you wrote,
Bill,

One of your criticisms is the chicken-egg conundrum of whether diet causes low HDL (or sex hormones), or whether cancers causes low HDL (or sex hormones?). What about skipping HDL (or sex hormones?), and going straight to diet-causing-cancer? ...
Ed, that is not one of my criticisms. You need to go back and read what I said more carefully. I said that a very low fat diet reduces the production of hormones, because it reduces cholesterol, which is involved in the manufacture of sex hormones. This is not a "conundrum"; it is a well known fact. Nor did I say that cancer causes low HDL, although it may; I said that it causes low total cholesterol. That too is not in dispute. For example, it is very obvious why liver cancer reduces cholesterol; the liver is the organ that produces cholesterol. The cancer causes the low cholesterol, because it impairs its production in the liver. Other forms of cancer reduce cholesterol as well, because the cancer eats away at the body. There is no evidence whatsoever that the reverse is true -- i.e., that low cholesterol causes cancer. Quite the contrary, for there is strong evidence that a macrobiotic diet, which is very low in fat and sugar (and therefore similar to the Pritikin diet), is anticarcinogenic.
Several recent epidemiological studies have shown an increase in breast cancer risk among women who have elevated plasma levels of testosterone, reduced levels of sex hormone-binding globulin (SHBG), and hence elevated levels of bioavailable androgens and estrogens not bound to SHBG. This endocrine profile is generally associated with obesity and chronic hyperinsulinemia, of which it is most likely a result. Lack of physical activity, obesity, and a diet rich in rapidly digestible carbohydrates and poor in fibre favour the development of insulin resistance and hyperinsulinemia.

Hyperinsulinemia and an increased IGF-I bioactivity could thus be an important physiological link between a western lifestyle, overnutrition, a hyperandrogenic sex steroid profile, and increased breast cancer risk.
Yes, but as I pointed out, hyperinsulinemia is due to insulin resistance, which in turn is caused by dietary fat, which interferes with the ability of insulin to metabolize the sugar. Studies have demonstrated that a diabetic condition can be produced in young healthy adults simply by feeding them a high-fat diet for two days and then giving them a glucose tolerance test in which they all score in the diabetic range. But if these same subjects are fed a high carbohydrate diet, containing sugar, candy, pastry, white bread, baked potatoes, syrup, bananas, rice and oatmeal, they all score in the normal range on the glucose tolerance test. The reason for the difference is very simple. Since the high-starch, high-sugar diet is free of fat, very little insulin is required to metabolize the sugar, which is cleared from the blood stream very quickly.
And what is the dietary pattern that results in chronic hyperinsulinemia? Answer: High-carb dieting (or a medium-high-carb diet alongside of a high trans, or saturated, fat intake).
Absolutely false! This is NOT what causes hyperinsulinemia. What causes hyperinsulinemia is a high-fat diet. A very low-fat diet will not give you hyperinsulinemia no matter how many sugary or starchy carbs you eat.

- Bill
(Edited by William Dwyer
on 3/03, 4:38pm)


Post 19

Friday, March 3, 2006 - 6:51pmSanction this postReply
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Ashley, If you are going to be taking fish oil supplements, you need to take a vitamin E supplement, as fish oil can cause a deficiency of vitamin E by up to 200 I.U.s. a day. I recall reading a study in a medical journal several years ago that documented this. It makes sense too, because fish oil is a highly unsaturated fatty acid that is easily subject to lipid peroxidation. In other words, it can go rancid very quickly, so you should make sure that the fish oil you are taking is fresh, that it is kept in a dark bottle and in a cool place once it is opened. You should also be taking vitamin E if you're taking vitamin C; the two work together to inhibit free radical damage. Another thing to keep in mind is that high doses of vitamin C (of 1,500 mg per day or more) can lower HDL levels by causing a deficiency of copper and altering copper/zinc ratios. One study in which subjects were supplemented with 4 grams of vitamin C a day for two months resulted in a 20% drop in HDL levels. This would probably not have occurred had they added a copper supplement. It's also important to make sure you're getting extra copper if you're taking a zinc supplement, as zinc increases your need for copper. Generally, a ratio of 1 part copper to 10 parts zinc is recommended.

Also, smoking will lower your HDL levels. What's most important, however, is LDL, which as Ed says, should definitely be below 130, and ideally below 100, although it's difficult to get it that low without a very low-fat diet. (For people who've had a heart attack, the current recommendation is to reduce LDL to 70 or less; only something like the Pritikin diet can get it that low). I can't get mine much below 100 even on the Pritikin diet. When I go off the diet, as I have occasionally, my LDL shoots up dramatically. So getting it below 70 is a tall order. Also HDL doesn't tell you very much without knowing the total cholesterol. With a very low total cholesterol (below 150), a low HDL is not a risk factor (except for smokers). As I mentioned, the Tarahuma Indians have average total cholesterols of 128 and average HDL levels of 34, and not a single case of heart disease in the entire population.

Ed, you mentioned that a 40 HDL is good and a 60 is great! Yes, that's the general consensus nowadays, but it can be very misleading, if your total cholesterol is high. You cannot treat HDL as having any special significance out of context -- apart from the factors causing it and independently of other cholesterol fractions. As Pritikin notes, HDL cholesterol can be raised both by healthy lifestyle habits such as exercise or by unhealthy practices such as alcohol consumption. Also, the kind of HDL that is raised by alcohol is different than that which is raised by exercise. Regardless of the reason for a high HDL, it won't protect you from heart disease. Marathon runner Jim Fixx had an HDL of 87. Alcohol was probably responsible for this above average level; otherwise, it's difficult to raise it above 60, even with sustained exercise, especially for men. Unfortunately, Jim died of a heart attack, because his total cholesterol (253) and LDL (159) were so high. His very high HDL didn't save him. Conversely, the Tarahumaras with an HDL that is 53 mg/dL LOWER than Jim Fixx's have no heart disease at all.

In addition to a high LDL, smoking increases your risk of atherosclerosis, so that even a low total cholesterol (or low LDL) is no guarantee of protection. The reason is that atherosclerosis is promoted by the oxidation of serum cholesterol, which is increased by smoking (as well as, of course, by polyunsaturated fat). Also, I would avoid egg noodles, as the cholesterol in the egg yolks is oxidized in the process of preparing the noodles. Vitamin E can protect against heart disease by preventing the oxidation of the LDL cholesterol. Most cholesterol is endogenous (produced by the liver from saturated fat), although cholesterol from food is still something to be concerned about. Pritikin recommends no more than 100 mg of dietary cholesterol per day.

- Bill


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