RoR: Forum

Bill,

Thanks for continuing to engage me, despite the observation that I can be "difficult" at times (my term, not yours). It is such a pleasure to engage you on this (read my comments in the other thread about engaging folks who desire truth).

I would like to come up with a name for our debate, something catchy. "The Great Nutrition Debate" is already taken, as it is the name for the conference that took place in 2000, where Atkins and Sears successfully defended low-carb dieting against Ornish, et al. Are you familiar with that one? The full transcript is available online.

Anyway, I will get back to you about your most recent points soon ...

Ed
[it appears we've both logged over a thousand hours in researching this aspect of reality -- we're champions meeting in the ring]

Post 21

Friday, March 3, 2006 - 9:48pm

Bill,

==============
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.
==============

Right. Low cholesterol hasn't been "shown" to "cause" cancer (it's only a biomarker). And yes, the macrobiotic diet is anticarcinogenic -- but for some reasons you fail to state. It's plant base ensures adequate things like anti-oxidants and fiber, which do reduce cancer -- along with it's low-sugar aspect. This is important: I'm not arguing for a plant-less diet, I'm arguing for a diet with approximately equal weights of plants and meat (say, 1-lb of meat per day, and 1-lb of fruits and veggies). and the Pritikin diet disallows for this research-backed "equal weight" dynamic.

==============
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.
==============

That's almost half-true. In her book, The Omega Diet, Artemis Simopoulos outlines 3 "proven ways" to induce insulin resistance ...

1) a diet high in refined carbohydrates
2) a diet low in omega-3 fatty acids/high in omega-6 fatty acids
3) a diet high in saturated and trans-fatty acids

And a fourth way is to induce various nutritional deficiencies, most notably chromium (references upon request). Here are some very recent, very relevant findings in support of my position on this matter ...

===============

The case for low carbohydrate diets in diabetes management. Nutr Metab (Lond). 2005 Jul 14;2:16.

Because carbohydrate is the major secretagogue of insulin, some form of carbohydrate restriction is a prima facie candidate for dietary control of diabetes. Evidence from various randomized controlled trials in recent years has convinced us that such diets are safe and effective, at least in short-term.

These data show low carbohydrate diets to be comparable or better than traditional low fat high carbohydrate diets for weight reduction, improvement in the dyslipidemia of diabetes and metabolic syndrome as well as control of blood pressure, postprandial glycemia and insulin secretion.

Furthermore, the ability of low carbohydrate diets to reduce triglycerides and to increase HDL is of particular importance. Resistance to such strategies has been due, in part, to equating it with the popular Atkins diet. However, there are many variations and room for individual physician planning.

Some form of low carbohydrate diet, in combination with exercise, is a viable option for patients with diabetes. However, the extreme reduction of carbohydrate of popular diets (<30 g/day) cannot be recommended for a diabetic population at this time without further study.

On the other hand, the dire objections continually raised in the literature appear to have very little scientific basis. Whereas it is traditional to say that more work needs to be done, the same is true of the assumed standard low fat diets which have an ambiguous record at best.

===============

The cardiovascular continuum in Asia--a new paradigm for the metabolic syndrome. J Cardiovasc Pharmacol. 2005 Aug;46(2):125-9.

In Asia, there is a trend toward an increase in the prevalence of the metabolic syndrome and cardiovascular disease. Abdominal adiposity is arguably the key factor underlying the development of insulin resistance and the metabolic syndrome. It is now known that adipose tissues secrete adipokines, and in obese subjects, there is a chronic low-grade inflammation.

The inflammation and the associated endothelial dysfunction are reversible in the early stages. The Asian diet is low in animal fat but high in carbohydrates. Recent studies suggest that low-carbohydrate diets are more effective than low fat diets in inducing weight loss, suggesting that excessive carbohydrate rather than fat is the cause of obesity.

Strategies to combat cardiovascular disease should now focus on tackling the epidemic of obesity and developing innovative and effective lifestyle and pharmacological interventions.

===============

Effects of dietary fats versus carbohydrates on coronary heart disease: a review of the evidence. Curr Atheroscler Rep. 2005 Nov;7(6):435-45.

Based on current evidence, replacement of total, unsaturated, and even possibly saturated fats with refined, high-glycemic index carbohydrates is unlikely to reduce CHD risk and may increase risk in persons predisposed to insulin resistance. In contrast, a diet that is 1) rich in whole grains and other minimally processed carbohydrates; 2) includes moderate amounts of fats (approximately 30%-40% of total energy), particularly unsaturated fats and omega-3 polyunsaturated fats from seafood and plant sources; 3) is lower in refined grains and carbohydrates; and 4) eliminates packaged foods, baked goods, and fast foods containing trans fatty acids, will likely reduce the risk of CHD.

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Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction. Nutr Metab (Lond). 2005 Nov 16;2:31.

Carbohydrate restriction is one of several strategies for reducing body mass but even in the absence of weight loss or in comparison with low fat alternatives, CHO restriction is effective at ameliorating high fasting glucose and insulin, high plasma triglycerides (TAG), low HDL and high blood pressure.

In addition, low fat, high CHO diets have long been known to raise TAG, lower HDL and, in the absence of weight loss, may worsen glycemic control. Thus, whereas there are numerous strategies for weight loss, a patient with high BMI and high TAG is likely to benefit most from a regimen that reduces CHO intake.

Reviewing the literature, benefits of CHO restriction are seen in normal or overweight individuals, in normal patients who meet the criteria for MetS or in patients with frank diabetes. Moreover, in low fat studies that ameliorate LDL and total cholesterol, controls may do better on the symptoms of MetS.

On this basis, we feel that MetS is a meaningful, useful phenomenon and may, in fact, be operationally defined as the set of markers that responds to CHO restriction. Insofar as this is an accurate characterization it is likely the result of the effect of dietary CHO on insulin metabolism.

Glucose is the major insulin secretagogue and insulin resistance has been tied to the hyperinsulinemic state or the effect of such a state on lipid metabolism. The conclusion is probably not surprising but has not been explicitly stated before. The known effects of CHO-induced hypertriglyceridemia, the HDL-lowering effect of low fat, high CHO interventions and the obvious improvement in glucose and insulin from CHO restriction should have made this evident.

In addition, recent studies suggest that a subset of MetS, the ratio of TAG/HDL, is a good marker for insulin resistance and risk of CVD, and this indicator is reliably reduced by CHO restriction and exacerbated by high CHO intake. Inability to make this connection in the past has probably been due to the fact that individual responses have been studied in isolation as well as to the emphasis of traditional therapeutic approaches on low fat rather than low CHO.

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Comparison of isocaloric very low carbohydrate/high saturated fat and high carbohydrate/low saturated fat diets on body composition and cardiovascular risk. Nutr Metab (Lond). 2006 Jan 11;3:7.

RESULTS : Percent fat mass loss was not different between diets VLCARB [very low carbohydrate diets] -4.5 +/- 0.5, VLF-4.0 +/- 0.5, HUF -4.4 +/- 0.6 kg). Lean mass loss was 32-31% on VLCARB and VLF [very low fat] compared to HUF [high unsaturated fat] (21%) (P < 0.05). LDL-C increased significantly only on VLCARB by 7% (p < 0.001 compared with the other diets) but apoB was unchanged on this diet and HDL-C increased relative to the other 2 diets.

Triacylglycerol was lowered by 0.73 +/- 0.12 mmol/L on VLCARB compared to -0.15 +/- 0.07 mmol/L on HUF and -0.06 +/- 0.13 mmol/L on VLF (P < 0.001). Plasma homocysteine increased 6.6% only on VLCARB (P = 0.026). VLCARB lowered fasting insulin 33% compared to a 19% fall on HUF and no change on VLF (P < 0.001).

The VLCARB meal also provoked significantly lower post prandial glucose and insulin responses than the VLF and HUF meals. All diets decreased fasting glucose, blood pressure and CRP (P < 0.05).

CONCLUSION : Isocaloric VLCARB results in similar fat loss than diets low in saturated fat, but are more effective in improving triacylglycerols, HDL-C, fasting and post prandial glucose and insulin concentrations. VLCARB may be useful in the short-term management of subjects with insulin resistance and hypertriacylglycerolemia.

===============

Low-carbohydrate diets: nutritional and physiological aspects. Obes Rev. 2006 Feb;7(1):49-58.

However, these undesirable effects may be counteracted with consumption of a low-carbohydrate, high-protein, low-fat diet, because this type of diet has been shown to induce favourable effects on feelings of satiety and hunger, help preserve lean body mass, effectively reduce fat mass and beneficially impact on insulin sensitivity and on blood lipid status while supplying sufficient calcium for bone mass maintenance.

===============

An update on low-carbohydrate, high-protein diets. Curr Opin Gastroenterol. 2006 Mar;22(2):153-9.

RECENT FINDINGS: Most studies demonstrate that subjects following low carbohydrate diets lose more weight over the first 3-6 months than subjects consuming control diets. This weight loss is not sustained, however, at 1 year. Carbohydrate controlled diets may be associated with increased insulin sensitivity and improved glycemic control.

High carbohydrate, low fat diets appear to have a more favorable impact on total and LDL cholesterol, whereas low carbohydrate diets have been shown to significantly decrease triglyceride and increase HDL cholesterol levels in short-term studies.

===============

Notable quote (regarding isocaloric substitutions):
VLCARB lowered fasting insulin 33% compared to a 19% fall on HUF and no change on VLF (P < 0.001).

Bottom Line:
Very low carbohydrate diets outperform very low fat diets with regard to hyperinsulinemia.

Ed

Post 22

Friday, March 3, 2006 - 10:29pm

Bill responding to Ashley ...

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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.
=============

Bill's right. Fish oil does increase E needs -- because E protects the oil from going rancid -- inside your body. In fact, in calculation of E needs, researchers look to polyunsaturated fat intake.

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You should also be taking vitamin E if you're taking vitamin C; the two work together to inhibit free radical damage.
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This is true, but it is more true the other way round (you should be taking C, if you take E). One reason for this is that C regenerates used-up (read: oxidized) E. Used-up E might hurt you (if no C is around to regenerate it!).

=============
(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).
=============

Ah, ah, ah, Bill. Native hunter-gatherers have LDLs this low -- and meat intake covers at least half of the total calories (and at least a fourth of the total weight) of their diets. Pritikin (ie. low-meat) diets aren't "necessary" -- as you claim.

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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. ...
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Bill, you're generalizing from a single case here. Stop doing that (it's bad epistemology).

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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.
=============

Right. Most cholesterol comes from our livers. However, I don't share your concern over dietary cholesterol. Here's relevant evidence to that ...

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Plasma LDL and HDL characteristics and carotenoid content are positively influenced by egg consumption in an elderly population1. Nutr Metab (Lond). 2006 Jan 6;3:6.

29 postmenopausal women (50-68 y) and 13 men (60-80 y) were assigned to either 3 eggs (EGG, 640 mg cholesterol/d) or an equal volume of cholesterol-free egg substitute (SUB, 0 mg cholesterol/d) for 30 d.

After EGG, hyper-responders had larger (>/= 21.2 nm) less atherogenic LDL particle (P < 0.001) and larger HDL particle (> 8.8 nm) (P < 0.01), with no significant difference in the total number of LDL or HDL particles. Regardless of response classification, all individuals had an increase in plasma lutein (from 32.4 +/- 15.2 to 46.4 +/- 23.3 ng/L) and zeaxanthin (from 8.8 +/- 4.8 to 10.7 +/- 5.8 ng/L) during EGG, yet hyper-responders displayed higher concentrations of carotenoids when compared to hypo-responders

CONCLUSION : These findings suggest that the increases in LDL-C and HDL-C due to increased egg consumption in hyper-responders are not related to an increased number of LDL or HDL particles but, to an increase in the less atherogenic lipoprotein subfractions. Also, increases in plasma carotenoids after EGG may provide a valuable dietary source for this population.
=============

Take away message:
3 whole eggs a day doesn't hurt -- and (by way of the increased antioxidants lutein and zeaxanthin) appears to help with human health.

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Dietary cholesterol provided by eggs and plasma lipoproteins in healthy populations. Curr Opin Clin Nutr Metab Care. 2006 Jan;9(1):8-12.

RECENT FINDINGS: The lack of connection between heart disease and egg intake could partially be explained by the fact that dietary cholesterol increases the concentrations of both circulating LDL and high-density lipoprotein (HDL) cholesterol in those individuals who experience an increase in plasma cholesterol following egg consumption (hyperresponders).

It is also important to note that 70% of the population experiences a mild increase or no alterations in plasma cholesterol concentrations when challenged with high amounts of dietary cholesterol (hyporesponders). Egg intake has been shown to promote the formation of large LDL, in addition to shifting individuals from the LDL pattern B to pattern A, which is less atherogenic.

Eggs are also good sources of antioxidants known to protect the eye; therefore, increased plasma concentrations of lutein and zeaxanthin in individuals consuming eggs are also of interest, especially in those populations susceptible to developing macular degeneration and eye cataracts.
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Take away message:
Eggs help your eyes.

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Maintenance of the LDL cholesterol:HDL cholesterol ratio in an elderly population given a dietary cholesterol challenge. J Nutr. 2005 Dec;135(12):2793-8.

The study followed a randomized crossover design in which subjects were assigned to consume the equivalent of 3 large eggs (EGG) daily or the same amount of a cholesterol-free, fat-free egg substitute (SUB) for a 1-mo period.

When all subjects were evaluated, there were significant increases in LDL cholesterol (LDL-C) (P < 0.05) and HDL-C (P < 0.001) for both men and women during the EGG period, resulting in no alterations in the LDL-C:HDL-C or the total cholesterol:HDL-C ratios.

In addition, the LDL peak diameter was increased during the EGG period for all subjects. In contrast, the measured parameters of LDL oxidation, conjugated diene formation, and LDL lag time did not differ between the EGG and the SUB periods. We conclude from this study that dietary cholesterol provided by eggs does not increase the risk for heart disease in a healthy elderly population.
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Take away message:
3 eggs per day, doesn't increase your heart disease risk (it more-than-likely reduces it -- by increasing LDL particle size).

Ed

Post 23

Saturday, March 4, 2006 - 12:02am

I wrote,

==============
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.
==============

Ed replied,

Right. Low cholesterol hasn't been "shown" to "cause" cancer (it's only a biomarker). And yes, the macrobiotic diet is anticarcinogenic -- but for some reasons you fail to state. It's plant base ensures adequate things like anti-oxidants and fiber, which do reduce cancer -- along with it's low-sugar aspect. This is important: I'm not arguing for a plant-less diet, I'm arguing for a diet with approximately equal weights of plants and meat (say, 1-lb of meat per day, and 1-lb of fruits and veggies). and the Pritikin diet disallows for this research-backed "equal weight" dynamic.

Ed, one pound of meat is unhealthy by any stretch of the imagination. I worry very much about your health, if you eat this much meat on a daily basis. You're a young guy now, but if you continue to eat this way, I can predict with virtual certainty that your health will be compromised as you get older. You're too nice a guy to harm yourself in this way. But if you insist on doing this, I encourage you to get your blood lipids tested on a regular basis. I used to eat a high meat, low carb diet, and my cholesterol was 250 at the age of 30, and my blood pressure was high as well, despite the fact that I was exercising. I am now 66 and my cholesterol is 100 points lower, and my blood pressure lower as well. I've lived both diets and have observed the results empirically. This is not some abstract theory for me. It is very much a concrete reality.

Furthermore, there is no doctor out there who is going to say that a total cholesterol of 250 is acceptable. It is not just heart disease that you have to worry about but cancer as well. A high meat diet has been implicated in colon and prostate cancer. And this kind of diet will thin your bones dramatically, because of all the protein your body has to eliminate. That much protein creates a negative calcium balance as your system seeks to neutralize the acidity in your blood by leeching calcium from your bones. Vegetarians at the age of 70 have stronger bones than meat eaters at the age of 50. This kind of diet is especially bad for women who are at much greater risk of osteoporosis as they get older. Your diet is also very hard on the kidney's, and could raise your blood pressure by impairing circulation. You should rethink this whole approach to diet. Studies were done back in the '60's with young 20-year old football players. One group was given a diet containing 100 grams of protein a day; the other group, 50 grams. The first group was found to be in negative calcium balance, even with an extra 1400 mg of calcium supplements per day, whereas the second group was not, even though it took no calcium supplements. But a pound of meat a day will give you more than 100 grams of protein. Do you really want to do this?? If I were going to do what you're doing, I would be especially vigilant in monitoring my blood pressure, and my blood lipids on a frequent basis. Btw, what is your lipid profile? When I used to work in a lab, I would get my blood tested on a regular basis, because it was free, and I did so in response to different diets, just to see the results. The Pritikin diet was the only one that lowered my cholesterol and blood pressure.

==============
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.
==============

That's almost half-true. In her book, The Omega Diet, Artemis Simopoulos outlines 3 "proven ways" to induce insulin resistance ...

1) a diet high in refined carbohydrates
2) a diet low in omega-3 fatty acids/high in omega-6 fatty acids
3) a diet high in saturated and trans-fatty acids

You are ignoring the study that I cited in which a diet high in refined carbohydrates did not induce insulin resistence, provided it was accompanied by an absence of fat for a period of at least two days.

I think a lot of these studies you cite are not sensitive enough to the effects of a very low fat diet. What they consider to be a low fat diet is probably around 20% of total calories or even higher, which is clearly not good enough. You need 10% of total calories or less for the diet to work.

And a fourth way is to induce various nutritional deficiencies, most notably chromium (references upon request). Here are some very recent, very relevant findings in support of my position on this matter ...

Right. I'm familiar with the importance of chromium in this regard.

As for the early hunter/gatherers having a 70 LDL, I'd like to see anyone get that low an LDL eating the kind of fatty meat that is available today. Can't be done.

- Bill

Post 24

Saturday, March 4, 2006 - 5:16pm

Bill,

=============
I've lived both diets and have observed the results empirically. This is not some abstract theory for me. It is very much a concrete reality.
=============

Bill, I applaud you on your personal success -- but I've said it once, and I'll say it again: generalization (of any physical phenomenon) from a single instantiation -- is bad epistemology. Looking at a single instance of something, doesn't tell you much about the surrounding "reality."

For instance, there's a genetic disorder called PKU (there's a warning about it on the label of diet sodas containing aspartame). If a person had PKU, then aspartame would hurt them -- but you can't generalize that to the greater population. It's bad epistemology. Nutrition is a normative thing, and you must look at the whole, to understand the parts sufficiently.

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Furthermore, there is no doctor out there who is going to say that a total cholesterol of 250 is acceptable.
=============

Ah, c'mon Bill -- when you make such flip-style arguments, you're just setting yourself up ...

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[Significance of cholesterol levels in patients 75 years or older] Yakugaku Zasshi. 2005 Nov;125(11):833-52.

From the age of 70 onward, total cholesterol levels decrease, perhaps associated with changes in the composition of some lipoprotein fractions. In subjects older than 75 years, being in the lowest quartile of cholesterol, insulinemia or serum albumin concentrations is associated with increased mortality. Cholesterol levels below 189 mg/dL in subjects older than 75 years should be considered an early sign of unidentified comorbidity or of rapid functional decline.

HDL cholesterol levels, rather than total or LDL cholesterol, were inversely associated with increased mortality from ischemic coronary disease and stroke appears to rise as HDL cholesterol levels fall, rather than total or LDL cholesterol. On the other hand, LDL concentrations below 106 mg/dL and HDL concentrations below 36 mg/dL were associated with an increased risk of death from infectious disease.

Stroke incidence, in particular, ischemic stroke, is highest in subjects older than 75 years. HDL cholesterol levels above 35 mg/dL appear to have a protective effect against ischemic stroke in subjects younger than 70 years. Two interventional drug studies investigating the effects of two statins (simvastatin and pravastatin) found that in subgroups of subjects older than 75 these drugs were associated with a reduction in all-cause mortality and cardiovascular morbidity, regardless of total cholesterol levels
=============

Summary:
In the elderly, total cholesterol below 189 is associated with risk, as are LDLs below 106 (and HDLs below 36). Also, the main beneficial effect of statins -- the most effective prescription meds for cholesterol reduction -- in reducing morality and morbidity, is not linked the drop in cholesterol.

And here comes the doozy ...

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[Need to change the direction of cholesterol-related medication--a problem of great urgency] Yakugaku Zasshi. 2005 Nov;125(11):833-52.

Graduate School of Pharmaceutical Sciences, Nagoya City University, Japan.

The cholesterol hypothesis implies that reducing the intake of saturated fatty acids and cholesterol and increasing that of polyunsaturated fatty acid are effective in lowering serum total cholesterol (TC), and thereby reducing the incidence of coronary heart disease (CHD). However, these dietary recommendations are essentially ineffective in reducing TC in the long run, but rather increase mortality rates from CHD and all causes.

The reported "apparent relative risk of high TC in CHD mortality" (the ratio of mortality at the highest/lowest TC levels) varied several-fold among populations studied. The incidence of familial hypercholesterolemia (FH) in a population was proposed to be a critical factor in the observed variability, which could be accounted for by assuming that 1) the high CHD mortality rate in high-TC groups is mainly a reflection of the incidence and severity of FH, and 2) high TC is not a causative factor of CHD in non-FH cases.

This interpretation is supported by recent observations that high TC is not positively associated with high CHD mortality rates among general populations more than 40-50 years of age. More importantly, higher TC values are associated with lower cancer and all-cause mortality rates among these populations, in which relative proportions of FH are likely to be low (circa 0.2%).

Although the effectiveness of statins in preventing CHD has been accepted in Western countries, little benefit seems to result from efforts to limit dietary cholesterol intake or to TC values to less than approximately 260 mg/dl among the general population and the elderly.

Instead, an unbalanced intake of omega6 over omega3 polyunsaturated fats favors the production of eicosanoids, the actions of which lead to the production of inflammatory and thrombotic lipid mediators and altered cellular signaling and gene expression, which are major risk factors for CHD, cancers, and shorter longevity.
=============

Summary:
Among general populations more than 40-50 years of age, "a total cholesterol of 250 is acceptible."

And I will marshall peer-reviewed counter-evidence to your other points when I have more time.

Ed

Post 25

Saturday, March 4, 2006 - 10:51pm

Bill and Ed:

I am away working this weekend and am just logging on to read this thread for the first time in a couple of days. I just want to say that I continue to be fascinated with this information and your grasp of the content, and I am going to print it out when I get home so I can read it more carefully and compare more easily. I am very appreciative of this information and can see that the supplement question was far more complicated than I knew.

Ash

Post 26

Sunday, March 5, 2006 - 6:50pm

Ashley,

Fascinating stuff, alright!

More later ...

Ed

Post 27

Sunday, March 5, 2006 - 9:22pm

Ed, I apologize for citing myself as an argument. You are correct. A single case is anecdotal and cannot stand by itself as adequate evidence. But I think it is legitimate to cite myself as a concrete example of what a large body of evidence already demonstrates for the general population. In that respect, I am not an anomaly, nor was Nathan Pritikin, who, when he discovered his diet, was in his 40's and was dying of heart disease and cancer, only to be given a new lease on life. You've already acknowledged that a macrobiotic diet (which is essentially what the Pritikin diet is, with a few modifications) is anti-carcinogenic as well as anti-atherogenic. The term "macrobiotic" means long life for a very good reason. Its health and longevity benefits are no longer in dispute. Nor is the predictive value of total cholesterol for coronary lesions. Below is evidence from the Framingham heart study, taken from the Cleveland Clinic for a population of 723 men, ages 17 to 39, in which significant (>50%) coronary lesions were found to be directly related to cholesterol level even within the "acceptable" limits of serum cholesterol:

Serum Cholesterol (mg/dl)______Significant lesions (>50%) % of Total Cases

<200 - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - 20%
201-225 - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - 38%
226-250 - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - 48%
251-275 - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - 60%
276-300 - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - 77%

This relationship would not by itself prove that high cholesterol causes coronary lesions were it not for our understanding of the precise mechanism by which this occurs. As I've mentioned in previous posts, correlation is not causation. Which brings me to your continued posting of the correlation between low cholesterol and diseases such as cancer, as if to argue that there the low cholesterol causes the disease. As I've pointed out repeatedly, the evidence is that the disease causes the low cholesterol, not the other way around. So it does no good to argue that high cholesterol is acceptable in an older population, because low cholesterol is associated with increased mortality. This is the fallacy of reversing cause and effect. And modern science is not immune to it, as the articles you're citing continue to demonstrate. Low cholesterol that results from dietary modification is not predictive of increased mortality; quite the contrary.

You state that total cholesterol of 250 is acceptable in an older population. Well, I'm almost 66, and my doctor has continued to congratulate me on my low cholesterol (150) and has cautioned me not to let it rise. I worked in a hospital for years, and what you're saying is not at all the consensus of the medical establishment. So I would be very careful as to what kind of conclusions you draw from the articles you've cited!

- Bill

Post 28

Sunday, March 5, 2006 - 9:44pm

Bill,

===============
But if you insist on doing this, I encourage you to get your blood lipids tested on a regular basis.
===============

I insist ...

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Carbohydrate rich diets exacerbate postprandial lipaemia in moderately dyslipidemic subjects, whereas red meat protein-enriched diets have no adverse effects. Asia Pac J Clin Nutr. 2004 Aug;13(Suppl):S52.

Subjects who consumed the high carbohydrate diet had no significant changes in fasting plasma lipids, glucose or insulin, however showed a doubling in the apolipoprotein B48 incremental area under the curve.

Conclusion - Chronic consumption of carbohydrate-enriched diets substantially increased arterial exposure to pro-atherogenic chylomicrons during the post-prandial state in moderately hypertriglyceridemic subjects.

[An apparent re-publication -- ( A low-protein diet exacerbates postprandial chylomicron concentration in moderately dyslipidaemic subjects in comparison to a lean red meat protein-enriched diet. Eur J Clin Nutr. 2005 Oct;59(10):1142-8. ) -- listed the utilized intervention] ...

INTERVENTION: Participants consumed an isocaloric weight maintenance diet low in protein (14, 53 and 30% of energy as protein, carbohydrate and fat, respectively) or high in protein (25, 35 and 30% energy as protein, carbohydrate and fat) for a period of 6 weeks.
===============

Bottom line:
High meat diets -- when total fat is kept low -- don't hurt (and might help).

You continued ...

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A high meat diet has been implicated in colon and prostate cancer.
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Not when a systematic review is performed on the totality of evidence (and distinction is made between processed meat and non-) ...

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Foodstuffs and colorectal cancer risk: A review. Clin Nutr. 2006 Feb;25(1):14-36. Epub 2005 Nov 14.

RESULTS: Twelve out of 15 studies found no significant relationship between vegetable intake and colorectal cancer risk; also, 11 out of 14 studies found no relationship with fruit consumption. Conversely, the combined consumption of vegetables and fruit reduced colorectal cancer risk in three out of six studies, although the relationship was somewhat inconsistent between genders and anatomical localizations.

Most studies found no relationship between cancer risk and red meat (15 in 20) or processed meat (seven out of 11) consumption ...
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... and ...

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Diet, anthropometric measures and prostate cancer risk: a review of prospective cohort and intervention studies. BJU Int. 2004 May;93(8):1139-50.

Intervention and prospective cohort studies support a protective role against prostate cancer for selenium, and possibly for vitamin E, pulses and tomatoes/lycopene. Overall consumption of meat, eggs, vegetables, fruit, coffee, tea, carotenoids and vitamins A, C and D was not consistently related to prostate cancer risk.
===============

Bottom line:
The totality of evidence does not point to an increased risk in these 2 cancers.

And finally ...

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And this kind of diet will thin your bones dramatically, because of all the protein your body has to eliminate. That much protein creates a negative calcium balance as your system seeks to neutralize the acidity in your blood by leeching calcium from your bones. Vegetarians at the age of 70 have stronger bones than meat eaters at the age of 50.
===============

That's not what I've read ...

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Nutritional treatment of bone fracture. Curr Opin Clin Nutr Metab Care. 2005 Jul;8(4):377-81.

A high protein intake was associated with a lower risk of hip fracture.
===============

... and ...

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Dietary protein: an essential nutrient for bone health. J Am Coll Nutr. 2005 Dec;24(6 Suppl):526S-36S.

In sharp opposition to experimental and clinical evidence, it has been alleged that proteins, particularly those from animal sources, might be deleterious for bone health by inducing chronic metabolic acidosis which in turn would be responsible for increased calciuria and accelerated mineral dissolution.

The main purpose of this review is to analyze the evidence that refutes a relation of causality between the elements of this putative patho-physiological "cascade" that purports that animal proteins are causally associated with an increased incidence of osteoporotic fractures. In contrast, many experimental and clinical published data concur to indicate that low protein intake negatively affects bone health.

In the elderly, low protein intakes are often observed in patients with hip fracture. In these patients intervention study after orthopedic management demonstrates that protein supplementation as given in the form of casein, attenuates post-fracture bone loss, increases muscles strength, reduces medical complications and hospital stay. In agreement with both experimental and clinical intervention studies, large prospective epidemiologic observations indicate that relatively high protein intakes, including those from animal sources are associated with increased bone mineral mass and reduced incidence of osteoporotic fractures.

As to the increased calciuria that can be observed in response to an augmentation in either animal or vegetal proteins it can be explained by a stimulation of the intestinal calcium absorption. Dietary proteins also enhance IGF-1, a factor that exerts positive activity on skeletal development and bone formation. Consequently, dietary proteins are as essential as calcium and vitamin D for bone health and osteoporosis prevention.
===============

... and ...

===============
[Osteoporosis diet] Ther Umsch. 2000 Mar;57(3):152-60.

Fiber and caffeine decrease calcium absorption from the gut and typically exert relatively minor effects, while sodium, protein and the acid/alkaline balance of the diet increase urinary excretion of calcium and are of much greater significance for the calcium homeostasis.

Alkali buffers, whether vegetables or fruits reverse this urinary calcium loss. As long as accompanied by adequate calcium intake, protein-rich diet is not deleterious to bone: a calcium-to-protein ratio of 20:1 (mg calcium/g protein) is recommended.
===============

Ed

Post 29

Sunday, March 5, 2006 - 10:09pm

You continued ...

=================
Your diet is also very hard on the kidney's, and could raise your blood pressure by impairing circulation.
=================

This is called the Brenner Hypothesis (that protein damages the kidney, ultimately leading to hypertension and kidney failure). It was outlined in 1986, and it has since been refuted ...

=================
Dietary protein restriction as a treatment for slowing chronic kidney disease progression: The case against (Review Article). Nephrology (Carlton). 2006 Feb;11(1):58-62.

(ii) most of the published randomised controlled trials demonstrate that low-protein diets do not significantly slow the rate of kidney disease progression; (iii) meta-analyses of controlled trials have demonstrated strong evidence of publication bias favouring studies with positive, rather than negative, results;
=================

... and ...

=================
Do regular high protein diets have potential health risks on kidney function in athletes? Int J Sport Nutr Exerc Metab. 2000 Mar;10(1):28-38.

To conclude, it appears that protein intake under 2. 8 g.kg does not impair renal function in well-trained athletes as indicated by the measures of renal function used in this study
=================

Comment:
2.8 g/kg is over 3 times the RDA for protein.

You continued ...

=================
Right. I'm familiar with the importance of chromium in this regard.
=================

But are you familiar with the increased chromium losses due to high carbohydrate dieting? ...

=================
Urinary chromium excretion and insulinogenic properties of carbohydrates. Am J Clin Nutr. 1990 May;51(5):864-8.

Glucose plus fructose was the most insulinogenic followed by glucose alone, starch plus fructose, starch alone, and water plus fructose. The urinary losses of chromium followed a similar pattern. Subjects with the highest concentrations of circulating insulin displayed decreased ability to mobilize chromium on the basis of urinary chromium excretion. Therefore, urinary chromium losses are related to the insulinogenic properties of carbohydrates.
=================

Bill, in an effort to reach some common ground, perhaps we can agree on this one issue: Diets should provide a low Glycemic (insulinogenic) Load?

Ed

(Edited by Ed Thompson on 3/05, 10:23pm)

Post 30

Sunday, March 5, 2006 - 11:09pm

Bill, thanks for the detailed response -- and Framingham (the largest ongoing study) is definitely a potential deal-breaker here.

==================
You've already acknowledged that a macrobiotic diet (which is essentially what the Pritikin diet is, with a few modifications) is anti-carcinogenic as well as anti-atherogenic. The term "macrobiotic" means long life for a very good reason.
==================

I never said it was anti-atherogenic! And macro- means "big," not "long." Big life, as in whole (unprocessed) foods -- heavy on the seaweeds, mind you. And you're still fighting back with flip quips, friend. Though that just makes our "convo" that much more fun for me, it's getting you into "rhetorical" pitfalls -- wouldn't you say?

==================
Its health and longevity benefits are no longer in dispute. Nor is the predictive value of total cholesterol for coronary lesions.
==================

What's in dispute is not absolute predictive value -- it is relative predictive value. If something is a better predictor, then it should be the primary concern. In this regard, "total cholesterol" doesn't hold a candle to the "total cholesterol-to-HDL" ratio -- in predictive value ...

==================
Search for an optimal atherogenic lipid risk profile: from the Framingham Study. Am J Cardiol. 2006 Feb 1;97(3):372-5.

The CHD risk increased stepwise two- to threefold in men and women from the first to third tertile of total/HDL cholesterol ratio, irrespective of the level of total or LDL cholesterol level. In men, the LDL cholesterol level reflected the lowest risk factor adjusted quintile 5 to quintile 1 relative risk (1.85), and the total/HDL cholesterol ratio predicted the greatest risk (relative risk 2.9).

In women, LDL cholesterol imparted the highest risk of the individual lipids (relative risk 3.9), and this was not exceeded by the lipid ratio (relative risk 3.8). In conclusion, the levels of components of the total/HDL cholesterol ratio have little influence on its prediction of CHD. In men, elevated LDL need not be treated aggressively if the total/HDL cholesterol ratio is low.
==================

... and this superiority is even true of congestive heart failure ...

==================
Incidence and epidemiology of heart failure. Heart Fail Rev. 2000 Jun;5(2):167-73.

About 19% of CHF cases have diabetes. It accounted for 6-12% of the CHF in the Framingham Study cohort. Dyslipidemia characterized by a high total/HDL cholesterol ratio, but not the total cholesterol alone was a risk factor for CHF.
==================

==================
As I've mentioned in previous posts, correlation is not causation. Which brings me to your continued posting of the correlation between low cholesterol and diseases such as cancer, as if to argue that there the low cholesterol causes the disease.
==================

Bill, give me more credit than that. In post 23, you quote me ...

==============
Right. Low cholesterol hasn't been "shown" to "cause" cancer (it's only a biomarker).
==============

... so I'd appreciate it if you'd integrate my explicit stance -- instead of some misleading insinuation of "causation" on my part. As if I'd try to pull one over on YOU! In short, you were saying that high total cholesterol is indicative of risk and I'm saying -- no, showing -- that it, by itself (ie. without a known HDL level), is not.

==============
Well, I'm almost 66, and my doctor has continued to congratulate me on my low cholesterol (150) and has cautioned me not to let it rise.
==============

This line of reasoning is guilty of the hasty generalization fallacy (or, in the least, the appeal to authority fallacy).

==============
I worked in a hospital for years, and what you're saying is not at all the consensus of the medical establishment.
==============

Well, I forget the fallacy -- but this line of reasoning is guilty, too.

==============
So I would be very careful as to what kind of conclusions you draw from the articles you've cited!
==============

Now, this one is all too easy to spot: argument from intimidation.

This post included, I've cited some of the best research out there, used systematic reviews when possible, and utilized multiple citations when not. Yeah, there's counter-evidence to my claims -- published out there. But I say that the counter-evidence doesn't epistemologically stack up -- and charge all opposition to prove me wrong. Now, there are 2 ways to prove me wrong:

1) Cite better evidence
2) Utilize superior reasoning (over the same evidence)

And, in my (young, naive?) mind, this has yet to be done.

Prove me wrong.

Ed
[That's my story ... and I'm sticking to it.]

Post 31

Monday, March 6, 2006 - 11:39am

Ed, pretty impressive list of article citations and counter-evidence. So, how do you explain the fantastic success of the Dean Ornish and Pritikin diets in reversing heart disease, because there is credible evidence that they do. And how do you explain the epidemiological evidence that populations following a very low fat vegetarian diet with total cholesterols of 100 to 140 have no heart disease? Are you suggesting that Pritikin's reversal of heart disease and concomitant remission of cancer had nothing to do with his dietary modifications, and that it was just pure unexplained coincidence?

I wonder if the studies you're citing in which the total cholesterol to HDL ratios are the best predictors of heart disease aren't relevant to populations with higher average cholesterol levels, and that when total cholesterol levels fall below 150, say, the ratio has less validity. The reason I say that is that my total cholesterol to HDL ratio is 5, but my doctor doesn't consider it to be a problem, because my total cholesterol and LDL are so low. Also, the Tarahumara have ratios around 4, but no heart disease, again the reason being their very low total cholesterol and LDL. Also, I wonder if the chylomicron influence of carbohydrate would be insignificant at lower levels of dietary fat. I noticed that the studies you cited all used diets of no less than 30% of fat as total calories. What would the results be at 10% of total calories?

I don't care for the manner in which theses studies are done, because they leave a lot unexplained. There is so much counter evidence out there to dispute these kinds of generalizations that I think much more rigorous studies need to be done. I'm not questioning the data; I'm questioning the interpretation of and generalizations from the data.

Sorry for suggesting that you were being disingenuous, but you've continued to cite articles that raise the point about an association between low cholesterol and increased mortality. If you're acknowledging the point I'm making about the cancer causing the low cholesterol (rather than the other way around), then what is the point of continuing to cite this kind of association? What good does it do to argue that high cholesterol is acceptable in an older population because low cholesterol is associated with increased mortality, if the association is one in which the diseases leading to the increased mortality cause the low cholesterol rather than the low cholesterol causing the diseases?

As to the assertion that high meat consumption poses a risk for prostate and colorectal cancer, I stand corrected. I'm no expert on this issue, so I can't debate the point. I was just reporting what I had read and heard from other sources. I wonder, though, if colorectal cancer has any correlation with fiber intake? Perhaps you could set me straight on that as well. Also, what have you learned about the possible causes of colorectal (and prostate) cancer other than antioxidant status? Is it strictly an issue of antioxidant consumption in the form of fruits and vegetables and various vitamins and minerals?

The information on high protein consumption NOT being associated with an increased risk of osteoporosis I find very surprising. I do know that in young women, a low calorie vegetarian diet (that is also low in protein) can reduce body fat to the point of amenorrhea and thereby predispose to fractures, but this is because the women are not getting enough calories to maintain healthy levels of body fat and estrogen. The association of fractures in elderly people on a low protein diet was surprising though. Evidently, a certain minimal level of protein is required for bone health. I had read, however, that vegetarians at the age of 70 have stronger bones than meat eaters at the age of 50. But the evidence you cite concerning the alkalyzing effects of fruits and vegetables is something I was not aware of. Interesting. I had read that a high phosphorous diet (e.g., a lot of cola drinks) can adversely affect bone health. Is that your understanding?

As regards high protein diets causing a negative calcium balance, some studies were done back in the 1960's that purportedly demonstrated this. I think I mentioned them in a previous post. What is one to make of that? Is it simply that the low protein group was eating more fruits and vegetables? Perhaps. I don't recall the other components of the diet being discussed.

As for agreeing on the fact that a low-glycemic diet is best, yes, probably, but remember the study I cited in which high glycemic foods eaten for two days on a no-fat diet produced very low blood sugar compared to high fat foods eaten for the same period of time? Do you deny that fat interferes with action of insulin in metabolizing the blood sugar? I do agree that postprandial glucose is higher on a high-carbohydrate diet than on a low one and also higher on a low-protein diet than on a higher one, if the carbohydrates are high glycemic. If they're low glycemic, then it shouldn't make much of a difference. On a glucose tolerance test, however, a high fat diet will yield a fasting glucose that is off the charts, whereas on a low fat diet, it will be within the normal range. So, if you're going to follow a high fat diet, you need to keep the carbs at a minimum, especially the high glycemic ones.

Also, I suspect that the glycemic index was developed by testing subjects who were already consuming a moderate to high-fat diet, and that the results would have been different if the tests of these various carbohydrates were done on subjects consuming a very low-fat diet. It is worth noting that different people have a different blood sugar response to the same foods, which could well be due to other dietary factors. Heredity may have something to do with it as well. Australian aborigines, for example, get a marked rise in blood sugar from the consumption of white potatoes, whereas the same food causes a much lower glucose response among Caucasians. Similarly, diabetes is much more common in native-American populations, which may not be due entirely to their high-fat, high-carbohydrate diets, even if the latter do play a role. These people probably evolved to handle a much lower calorie, lower glycemic diet by using carbohydrate and calories more efficiently. So when they were exposed to the higher calorie, higher glycemic diet of the Europeans, their systems couldn't handle it.

- Bill

P.S. This edit corrects an error that I made in stating that vegetarians at the age of 50 have stronger bones than meat eaters at the age of 70. Of course, I intended to say just the opposite! :-P

(Edited by William Dwyer
on 3/06, 11:49am)

(Edited by William Dwyer
on 3/06, 6:28pm)

Post 32

Monday, March 6, 2006 - 8:20pm

Bill, thanks for the poignant questions. I will get around to answering them soon.

One of the key points that prevents our coming to terms on several issues, is the paucity of human data on 10% fat diets (because folks won't stay on them -- and the high attrition kills generalizability).

So your standard comeback has become: "But if they were only on a 10% fat diet, then ... "

Respectful Request:
Please direct me to some published research on 10% fat diets, Bill.

Ed

Post 33

Tuesday, March 7, 2006 - 12:46am

For more than 40 years, Dr. James Barnard has studied the role of diet and exercise in preventing and controlling diseases that are epidemic in industrialized societies. His more than 100 studies on the Pritikin Program, an approach that advocates daily aerobic activity and a low-fat eating plan rich in unrefined carbohydrates like fruits, vegetables, and whole grains, have been published in peer-reviewed journals such as the Archives of Internal Medicine, Diabetes Care, and the New England Journal of Medicine. They have documented the results of the Pritikin Program, which include:

� Reducing virtually all heart disease risk factors including cholesterol, triglycerides, inflammatory markers like C-reactive protein, and insulin levels
� Lowering blood pressure to normal, medication-free levels
� Controlling diabetes and, for many, eliminating the need for drugs and insulin injections
� Eliminating the need for angioplasty and bypass surgery and relieving angina pain
� Reducing key risk factors for breast, colon, and prostate cancer

Because of his groundbreaking research, Dr. Barnard has received numerous honors and awards, including the President�s Lecturer, American College of Sports Medicine National Meeting, 1995; and the Cureton Tutorial Lecture, American College of Sports Medicine National Meeting, 2002.

Over the past three decades, Dr. Barnard has been awarded more than 20 research grants from several nonprofit health organizations, including the National Institutes of Health, the American Heart Association, and the Nathan Pritikin Research Foundation.

Dr. Barnard has presented his research at more than 90 health conferences worldwide, including the International Cancer Conference in Switzerland (2004), the Jonsson Cancer Center at UCLA School of Medicine (2004), and the American Association for Cardiopulmonary Rehabilitation National Meeting in Kansas City (2003). In 2004and 2005, he presented data at the American Heart Association�s national conference showing reductions in LDL cholesterol, trigylcerides, and excess weight achieved by children following the Pritikin Program.

UCLA Scientists Report Pritikin� Diet/Exercise Program Dramatically Lowers Inflammation And Heart Attack Risk Factors

AVENTURA, Fla., Feb. 4 -- In a study released in this month's issue of the journal "Metabolism", UCLA scientists report that the Pritikin diet, low in fat and high in fruits, vegetables, and whole grains, augmented with daily exercise, significantly reduced C-reactive protein levels in study participants.

Last year, the American Heart Association added C-reactive protein testing as a leading assessment tool in determining heart attack risk. High levels of C-reactive protein (CRP) in the blood indicate inflammation in blood vessel walls. Scientists now suspect that coronary-artery inflammation plays a key role in making fatty deposits in the artery vulnerable to rupture, a leading cause of heart attacks. In fact, high CRP levels may be a better predictor of heart attacks than cholesterol levels, according to new research led by Harvard professor Dr. Paul Ridker of Brigham and Women's Hospital in Boston.
With the increasing concern over heart disease in women (it is the #1 killer of women over 50), CRP testing may be of particular benefit. A recently published study from Harvard University on 28,000 women found that those with the highest CRP levels were twice as likely to suffer heart problems as those with high LDL bad cholesterol.

In the new study, the UCLA team, lead by Dr. James Barnard, UCLA Department of Physiological Science, measured "entry and exit" blood values of 20 women, ages 51 to 79 years, attending a two-week program at the Pritikin Longevity Center�. All had multiple risk factors for heart disease, including obesity, hypertension, and diabetes.

At Pritikin, the women exercised daily and ate a diet focused on high- fiber carbohydrates such as fruits, vegetables and whole grains. Their diet also included lean, calcium-rich foods like nonfat milk and small, lean servings of seafood, poultry, and red meat. The women were encouraged to eat until they were full.

In just two weeks, CRP levels plunged, on average, 45%. There were also major reductions in LDL cholesterol (19%), total cholesterol (17%), insulin (26%), glucose (11%), and triglycerides (15%).

Concludes Dr. Barnard: "We know that inflammation is a key problem, a leading cause of heart disease, and now we're learning that diet and exercise plans like the Pritikin Program may be a safe, smart solution. In fact, no other diet-and-exercise program or drug therapy, including statins, has proven to lower C-reactive protein levels so dramatically -- or so rapidly."

Dean Ornish did a study involving 48 patients randomly divided into two groups. One group followed Ornish�s 10% of total calories as fat diet, and the other group followed the advice of their physicians, which included modest reductions in fat and cholesterol. The patients who followed the Ornish progam had an average of 91% reduction in the amount of chest pain (angina), a 55 percent improvement in exercise capability, a 21 percent reduction in cholesterol levels, and significant reductions in blood pressure at rest and during emotional stress � all after only 24 days on the diet. Using a nuclear medicine test, called a gated blood pool scan, the researchers measured overall improvements both in the ability of the heart to pump blood and in how uniformly it was contracting, two indirect indications that the heart disease was improving. All of these improvements were statistically significant compared with the other group, whose heart disease either stayed the same or became slightly worse during the same time interval. The study was published in JAMA (Ornish DM, et al. �Effects of stress management training and dietary changes in treating ischemic heart disease.� JAMA. 1983; 249:54-59.)

In another similar study, patients with severe coronary heart disease were randomly divided into two groups. One group was put on the Ornish diet (10% of total calories as fat); the other group was asked to make moderate dietary changes (eat less red meat, more fish and chicken, margarine instead of butter and no more than three eggs per week), to exercise moderately, and to quit smoking. After only one year, the majority (82%) of the Ornish group demonstrated measurable average reversal of their coronary artery blockages. (Not every blockage in each artery was reversed, but the majority were.) Overall, the average blockage reversed from 61.1 to 55.8 percent; more severely blocked arteries showed even greater improvement. These blockages took decades to build up in the arteries, so they don�t just melt away completely in only a year. But even a small amount of reversal after one year in a severely blocked artery causes a great improvement in blood flow to the heart (as measured by a cardiac PET scan). In contrast, the majority of the heart patients in the comparison group became measurably worse during the same interval. These findings were published in the Lancet (the most well-respected international medical journal). (Ornish, et al., �Can lifestyle changes reverse coronary heart disease? The Lifestyle Heart Trial.� Lancet, July 21, 1990).

Ornish has two diets: the reversal diet and the prevention diet. On the reversal diet, which is what the participants in these studies were on, all animal products (with the exception of nonfat milk, nonfat yogurt, egg whites, or products made from these) are excluded. That means no meats, poultry, seafood or egg holks. Also excluded are vegetarian foods that are high in fat: all oils (except in very small quantities), nuts, seeds, avocados, chocolate and other cocoa products, olives, and coconut.

PROSTATE CANCER

Led by Dr. Michael Freeman at Children�s Hospital Boston, scientists injected human prostate cancer cells into mice. They fed half the mice a high-fat, high-cholesterol diet. In these mice, blood cholesterol levels shot up, and, observed the scientists, cholesterol accumulated in the outer membranes of the tumor cells, activating a chemical �cell-survival� pathway called Akt, which has been found to help tumors survive and thrive.

Six weeks after the tumor cells were injected, the incidence of tumors more than doubled in the mice on the high-fat, high-cholesterol diets. Activation of Akt, Dr. Freeman and his team concluded, enabled the tumor cells to resist chemical cues that trigger apoptosis (programmed cell death).

These new findings echo previous research on populations that have linked prostate cancer with high levels of cholesterol in the blood as well as with Western diets high in cholesterol - and saturated fat-rich foods like red meat and full-fat dairy products.

They also mirror research from UCLA scientist Dr. James Barnard. When Dr. Barnard and his team mixed blood samples of men on a typical high-fat, high-cholesterol American diet in dishes with prostate cancer cells, the cancer cells grew vigorously. Fewer than 3% showed apoptosis. When blood samples of these same men were tested after they had completed two weeks at the Pritikin Longevity Center, close to 40% of the prostate cancer cells had died off.**

States Dr. Barnard: �There�s every reason to believe that if you catch prostate cancer early on and adopt the Pritikin Program, you can significantly increase your odds of living your life free of invasive prostate cancer.�

DIABETES

Three-week Diet-Exercise Study Shows 50 Percent Reversal In Metabolic Syndrome, Type 2 Diabetes
Abstract

Obese and overweight individuals suffering metabolic syndrome and Type 2 diabetes showed significant health improvements after only three weeks of diet and moderate exercise even though the participants remained overweight.
Complete Article
24 Jan 2006

"The study shows, contrary to common belief, that Type 2 diabetes and metabolic syndrome can be reversed solely through lifestyle changes," according to lead researcher Christian Roberts of University of California, Los Angeles.

"This regimen reversed a clinical diagnosis of Type 2 diabetes or metabolic syndrome in about half the participants who had either of those conditions. However, the regimen may not have reversed damage such as plaque development in the arteries," Roberts said. "However, if Type 2 diabetes and metabolic syndrome continue to be controlled, further damage would likely be minimized and it's plausible that continuing to follow the program long-term may result in reversal of atherosclerosis."

"The results are all the more interesting because the changes occurred in the absence of major weight loss, challenging the commonly held belief that individuals must normalize their weight before achieving health benefits," Roberts said. Participants did lose two to three pounds per week, but they were still obese after the 3-week study.

The study, "Effect of a diet and exercise intervention on oxidative stress, inflammation, MMP-9, and monocyte chemotactic activity in men with metabolic syndrome factors," is in the online edition of the Journal of Applied Physiology published by the American Physiological Society. Researchers were Christian K. Roberts, Dean Won, Sandeep Pruthi, Silvia Kurtovic, and R. James Barnard, all of UCLA; Ram K. Sindhu of Charles R. Drew University, Los Angeles; and Nosratola D. Vaziri of University of California, Irvine.

The study involved 31 men who ate a high-fiber, low-fat diet with no limit to the number of calories they could consume. The participants also did 45-60 minutes of aerobic exercise per day on a treadmill.

Fifteen of the men had metabolic syndrome, a condition that is characterized by excessive abdominal fat, insulin resistance, and blood fat disorders such as high levels of triglycerides (fat in the blood) or low levels of HDL (high density lipoprotein, or "good" cholesterol). Thirteen of the participants had Type 2 diabetes. There was also some overlap between the two groups and some participants who had neither metabolic syndrome nor Type 2 diabetes, but were overweight or obese.

"The diet, combined with moderate exercise, improved many factors that contribute to heart disease and that are indirect measures of plaque progression in the arteries, including insulin resistance, high cholesterol, and markers of developing atherosclerosis," Roberts said. "The approach used in this experiment of combining exercise with a diet of unlimited calories is unusual."

Low-calorie foods

The participants in the current study, who ranged in age from 46 to 76 years old, took part in a 21-day residential program at the Pritikin Longevity Center, formerly in Santa Monica, combining the Pritikin diet and exercise program. The daily diet was low fat (12-15% of calories), moderate protein (15-20% of calories), and high in unrefined carbohydrates (65-70% of calories) and fiber (more than 40 grams).

Natural foods - whole grains (five or more servings daily), vegetables (four or more servings), and fruits (three or more servings) - were the main source of daily carbohydrates. The sources of protein were plants (such as soy, beans, and nuts), nonfat dairy (up to two servings daily), and fish and poultry (3.5-ounce portion once a week and in soups and casseroles twice a week). The remainder of the calories came from fat with a polyunsaturated-to-saturated fatty acid ratio of 2.4 to 1.

"Aside from meat and dairy, the study participants could eat as much as they wanted," Roberts said. "Because the food was not as high calorie as a typical American diet, the participants ate less before feeling full. This is a departure from most diets, which usually leave the dieter feeling hungry," he said.

The men also exercised daily on a treadmill, including level and graded walking, for 45-60 minutes. The exercise program was tailored to ensure each individual reached 70-85% of maximum heart rate.

Next steps

Trials outside the laboratory environment are needed to test the regimen in the general population. "The findings are likely generalizable, although the magnitude of change is proportional to the degree of abnormality when the person begins the regimen," Roberts added.

Scientists also need to determine whether long-term lifestyle change can prevent or reverse end-organ damage noted in those with metabolic syndrome or Type 2 diabetes, Roberts said. These changes may be difficult to make but the payoff for individuals and society could be enormous.

Further studies are also needed in those who are at risk for metabolic syndrome or Type 2 diabetes. Individuals should still be tested to see if Type 2 diabetes and metabolic syndrome can be prevented in the first place. Individuals may be considered healthy before developing metabolic syndrome but looking healthy does not necessarily mean being healthy, he noted.

(Source: American Physiological Society: January 2006.)

Post 34

Tuesday, March 7, 2006 - 8:14am

Bill,

A problem I have on published research regarding really low fat diets is that comprehensive lifestyle change almost always accompanies them. Making comprehensive changes obscures effect-attribution (there's no way to tell if the diet helped, or not -- because too many changes were made).

An example of this is the "landmark" study by Ornish -- where folks were held in a lifestyle commune, with anti-smoking plans, stress management, and directed exercise (along with diet). You can't generalize (about diet) from studies like that -- it's just bad epistemology.

Workable if we're all willing to live in strict communes, though.

Ed

Post 35

Tuesday, March 7, 2006 - 9:37am

Ed, it's reasonable to infer that diet contributed to the changes, because we already have supporting evidence from clinical and epidemiological studies, as well as from primate studies in which similar dietary changes produced a regression of atherosclerosis in monkeys. You could, of course, argue that monkeys are not human beings, and so we can't infer anything from that either. The thing that's nice about the primate studies, though, is that they isolate the purely physical effects of diet from those of exercise and stress management, which lends support to the contribution of the dietary component apart form these other lifestyle changes.

- Bill

Post 36

Wednesday, March 8, 2006 - 12:13pm

Bill,

You wrote ...
================
For more than 40 years, Dr. James Barnard has studied the role of diet and exercise in preventing and controlling diseases that are epidemic in industrialized societies. His more than 100 studies on the Pritikin Program
================

Well, looking at the last 40 years of his publications, he doesn't have over 100 "peer-reviewed" studies on the Pritikin Program. He's got 92 peer-reviewed studies in total (from 1966-2006), and most of them are not on this program, or low-fat diets in general. And I bring this up because you've over-stated the case.

You wrote ...
================
UCLA Scientists Report Pritikin� Diet/Exercise Program Dramatically Lowers Inflammation And Heart Attack Risk Factors

AVENTURA, Fla., Feb. 4 -- In a study released in this month's issue of the journal "Metabolism", UCLA scientists report that the Pritikin diet, low in fat and high in fruits, vegetables, and whole grains, augmented with daily exercise, significantly reduced C-reactive protein levels in study participants.
================

Well, while body weight is the heaviest factor in determining C-reactive protein, high-fat diets lower it better than low-fat diets do ...

================
Effect of a mediterranean-style diet on endothelial dysfunction and markers of vascular inflammation in the metabolic syndrome: a randomized trial. JAMA. 2004 Sep 22;292(12):1440-6.

INTERVENTIONS: Patients in the intervention group (n = 90) were instructed to follow a Mediterranean-style diet and received detailed advice about how to increase daily consumption of whole grains, fruits, vegetables, nuts, and olive oil; patients in the control group (n = 90) followed a prudent diet (carbohydrates, 50%-60%; proteins, 15%-20%; total fat, <30%).

Compared with patients consuming the control diet, patients consuming the intervention diet had significantly reduced serum concentrations of hs-CRP (P =.01), IL-6 (P =.04), IL-7 (P = 0.4), and IL-18 (P = 0.3), as well as decreased insulin resistance (P<.001). Endothelial function score improved in the intervention group (mean [SD] change, +1.9 [0.6]; P<.001) but remained stable in the control group (+0.2 [0.2]; P =.33). At 2 years of follow-up, 40 patients in the intervention group still had features of the metabolic syndrome, compared with 78 patients in the control group (P<.001).
================

... and, if you want to quibble about the LEVEL of fat in the "low-fat" diet, then I'll just marshall the following evidence ...

================
METHODS: Sixteen overweight subjects who were 46 +/- 14 y old were placed on a weight-maintaining baseline diet consisting of 35% fat, 45% carbohydrate, and 20% energy as protein. After 2 wk, subjects were switched to an isocaloric low-fat diet consisting of 15% fat, 65% carbohydrate, and 20% protein for another 2 wk. For the final 12 wk of the study, subjects consumed the same 15% fat diet ad libitum. At the end of each diet phase, CRP was measured by a high-sensitivity CRP assay.

RESULTS: The weight of subjects remained stable during the first 4 wk of isocaloric diets. Plasma CRP concentrations after 2 wk on the weight-maintaining 35% fat diet and 2 wk on the isocaloric 15% fat diet were not significantly different (median +/- interquartile range 1.42 +/- 3.30 and 1.59 +/- 3.29 mg/L, respectively).
================

Summary:
Going from a 35% fat diet to a 15% diet non-significantly increased C-reactive protein.

You wrote ...
================
PROSTATE CANCER

Led by Dr. Michael Freeman at Children�s Hospital Boston, scientists injected human prostate cancer cells into mice. They fed half the mice a high-fat, high-cholesterol diet. In these mice, blood cholesterol levels shot up, and, observed the scientists, cholesterol accumulated in the outer membranes of the tumor cells, activating a chemical �cell-survival� pathway called Akt, which has been found to help tumors survive and thrive.

[break]

These new findings echo previous research on populations that have linked prostate cancer with high levels of cholesterol in the blood as well as with Western diets high in cholesterol - and saturated fat-rich foods like red meat and full-fat dairy products.

They also mirror research from UCLA scientist Dr. James Barnard.
================

Well, for one thing, dairy products are linked to prostate cancer -- but "full-fat dairy" is shamefully misleading here ...

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Dairy, calcium, and vitamin D intakes and prostate cancer risk in the National Health and Nutrition Examination Epidemiologic Follow-up Study cohort. Am J Clin Nutr. 2005 May;81(5):1147-54.

RESULTS: Compared with men in the lowest tertile for dairy food intake, men in the highest tertile had a relative risk (RR) of 2.2 (95% CI: 1.2, 3.9; trend P = 0.05). Low-fat milk was associated with increased risk (RR = 1.5; 95% CI: 1.1, 2.2; third compared with first tertile; trend P = 0.02), but whole milk was not (RR = 0.8; 95% CI: 0.5, 1.3; third compared with first tertile; trend P = 0.35). Dietary calcium was also strongly associated with increased risk (RR = 2.2; 95% CI: 1.4, 3.5; third compared with first tertile; trend P = 0.001).
================

Summary:
Low-fat milk was associated with statistically-significantly increased risk for prostate cancer -- while whole milk (ie. "full-fat milk") was not; and it was actually associated with a non-significant 20% reduction in risk. And, on higher-fat (lower carb) dieting ...

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Nutritional factors and prostate cancer: a case-control study of French Canadians in Montreal, Canada. Cancer Causes Control. 1996 Jul;7(4):428-36.

No association was evident between energy intake and the risk of prostate cancer. In contrast, there was some evidence of an inverse association with intake of total fat, animal fat, monounsaturated fat, and particularly saturated fat (odds ratio = 0.69, 95 percent confidence interval = 0.40-1.18, P = 0.05), while a nonsignificant positive association was found with polyunsaturated fat.
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And a biochemical explanation for these findings ...

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Are diet-prostate cancer associations mediated by the IGF axis? A cross-sectional analysis of diet, IGF-I and IGFBP-3 in healthy middle-aged men. Br J Cancer. 2003 Jun 2;88(11):1682-6.

We examined the association of diet with insulin-like growth factors (IGF) in 344 disease-free men. Raised levels of IGF-I and/or its molar ratio with IGFBP-3 were associated with higher intakes of milk, dairy products, calcium, carbohydrate and polyunsaturated fat; lower levels with high vegetable consumption, particularly tomatoes.
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Ed
[and I'll have to tackle diabetes in another post -- that one's going to be a mother-load)

Post 37

Wednesday, March 8, 2006 - 1:40pm

Continuing with the epidemiological evidence, Henry Blackburn wrote an article, "The public health view of diet and mass hyperlipidemia. (Cardiovascular. Rev. Rep., Aug. 1980, 433-42: Sept. 1980, 361-69.) whose main thesis, according to Nathan Pritikin, can be summarized in three sentences: "Atherosclerotic CHD is a public health phenomenon of affluent cultures. Population comparisons suggest that mass hyperlipidemia is a prime requisite for mass atherosclerosis. On the basis of available evidence, the habitual diet of a culture is, in turn, the chief factor leading to hyperlipidemia." Blackburn divides the world into four categories according to average cholesterol levels, as shown in the following Table:

Relationship of Mean Population Cholesterol Level and Incidence of Atherosclerosis

Mean population cholesterol level (mg/dl)______Incidence of atherosclerosis
_______________120_______________________________Rare___________
_______________160_______________________________Minimal________
_______________190_______________________________Reduced________
_____________220-280_____________________________Epidemic_______

Another interesting piece of evidence is that during World War II, in Europeans who were not able to get butter, meat and cheese, there was a dramatic drop in heart attacks, and this was among people who were under the constant stress of being bombed. So stress reduction is probably less of a factor in atherosclerotic regression than diet is. Similarly, exercise is not the panacea that it's often made out to be. A five-year study done at Methodist Hospital in Houston reports that a large proportion of men, aged 40 to 60, who were long-distance runners developed evidence of coronary heart disease.

The 41 subjects in the study had been marathon runners for at least two years before the study began. At the beginning of the investigation, 5 men had positive (abnormal) stress tests; by the end of the third year, 13 had developed positive tests; by the five-year mark, 18 recorded positive stress tests. Furthermore, when those runners who tested abnormal were checked with the normal runners, there was no difference in average miles run per year, age, cholesterol, or endurance. Heart disease gradually evolved in all of the subjects, and in time most of them would show an abnormal stress test, followed by heart attack, angina, and death. Evidently, it is the dietary component that was most significant in the regression of atherosclerosis among the subjects in the studies cited earlier.

Here is another interesting table from the Framingham Heart Study and Chicago Heart Association:

Cholesterol Level (mg/dl)________________Relative Risk of:__Developing Heart Disease___&___Dying of Heart Disease________
__________________________________________________________Framingham Study*___________Chicago Heart Assoc.**________
_______140-159________________________________________________1_______________________________1___________________
_______160-179_______________________________________________________________________________4.5___________________
_______195-218___________________________________________5.3_________________________6.3___________________
_______219-240___________________________________________6.7_________________________7.5___________________
_______241-268__________________________________________12.4_________________________8.5___________________
_______268_+____________________________________________15.3________________________16.8__________________

People who switch to a diet that 10% of total calories as fat drop their total cholesterol significantly. Pritikin dropped his from over 300 to 120. I dropped mine from 185 to 115. A friend of mine dropped his so much that his doctor was amazed (I forget the exact number). Another friend of mine who was diabetic dropped her fasting glucose down into the normal range and eliminated her need for insulin on the Pritikin low-fat, high carbohydrate diet.

To say, as the title of this thread does that "low-fat diets are stupid and potentially dangers" is hyperbolic nonsense in view of all the good that the Pritikin diet has done for people's health since its inception. We all owe a debt of gratitude to it's founder and to the people who are now carrying on his pioneering work, such as Dean Ornish and John McDougall. But the real credit goes to Nathan Pritikin, the man who healed America's heart!

- Bill

Post 38

Wednesday, March 8, 2006 - 8:49pm

Wow, Bill! The "man who healed America's heart" ... nice polemic, though.

By the way, MacDougall is a madman. That man would have us all on less than 10% protein, if he could. I have intellectually ripped his arguments to shreds (revealing his intellectual dishonesty)

Now, just a couple of posts ago, I showed that the total/HDL ratio is TWICE as predictive of CVD risk as total cholesterol is -- yet you continue on with a spiel regarding total cholesterol. More importantly, the study showing this doubling of predicive power -- was based on the Framingham Study.

For what it's worth -- some peer-reviewed evidence on type 2 diabetes, carbs, and fats:

Fetal Programming (in rats) ...
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Neonatal nutrition: metabolic programming of pancreatic islets and obesity. Exp Biol Med (Maywood). 2003 Jan;228(1):15-23.

In this context, the consequences of a high carbohydrate (HC) dietary intervention in neonatal rats is being studied in our laboratory. Artificial rearing of 4-day-old rat pups on a HC milk formula up to Day 24 results in the immediate onset of hyperinsulinemia, which persists throughout the period of dietary intervention.

Collectively, our results indicate that even a mere switch in the nature of the source of calories (from fat rich in rat milk to carbohydrate rich in the HC milk formula) during critical phases of early development in the rat results in metabolic programming of islet functions leading to chronic hyperinsulinemia (throughout life) and adult-onset obesity.

This metabolic programming, once established, forms a vicious cycle because HC female rats spontaneously transmit the HC phenotype to their progeny.
=================

Summary:
Replacing a high-fat diet (for pregnant mother rats) with a high-carbohydrate diet condemns her offspring to what some researchers now call: Diabesity.

Battle of the diets (less carbs, more protein -- less diabetes) ...
=================
Comparison of high-fat and high-protein diets with a high-carbohydrate diet in insulin-resistant obese women. Comparison of high-fat and high-protein diets with a high-carbohydrate diet in insulin-resistant obese women. Diabetologia.>Diabetologia. 2005 Jan;48(1):8-16.

However there is widespread interest in high-fat ("Atkins Diet") and high-protein ("Zone Diet") alternatives to the conventional high-carbohydrate, high-fibre approach. We report on a randomised trial that compared these two alternative approaches with a conventional diet in overweight insulin-resistant women.

RESULTS: Body weight, waist circumference, triglycerides and insulin levels decreased with all three diets but, apart from insulin, the reductions were significantly greater in the HF and HP groups than in the HC group. These observations suggest that the popular diets reduced insulin resistance to a greater extent than the standard dietary advice did.

When compared with the HC diet, the HF and HP diets were shown to produce significantly (p<0.01) greater reductions in several parameters, including weight loss (HF -2.8 kg, HP -2.7 kg), waist circumference (HF -3.5 cm, HP -2.7 cm) and triglycerides (HF -0.30 mmol/l, HP [corrected] -0.22 mmol/l).

LDL cholesterol decreased in individuals on the HC and HP diets, but tended to fluctuate in those on the HF diet to the extent that overall levels were significantly lower in the HP group than in the HF group (-0.28 mmol/l, 95% CI 0.04-0.52, p=0.02). Of those on the HF diet, 25% showed a >10% increase in LDL cholesterol, whereas this occurred in only 13% of subjects on the HC diet and 3% of those on the HP diet.

CONCLUSIONS/INTERPRETATION: In routine practice a reduced-carbohydrate, higher protein diet may be the most appropriate overall approach to reducing the risk of cardiovascular disease and type 2 diabetes.
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Glycemic Load is a deal breaker ...
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Glycemic index, postprandial glycemia and cardiovascular disease. Curr Opin Lipidol. 2005 Feb;16(1):69-75.

RECENT FINDINGS: In ecological studies, average dietary glycemic index (a measure of the postprandial glycemic potential of carbohydrates) and glycemic load (average glycemic index x amount of carbohydrate) predicts coronary infarct and cardiovascular disease risk factors, including HDL cholesterol, triglycerides and C-reactive protein.

In short-term intervention studies of overweight and hyperlipidemic patients, low glycemic index diets lead to improvements in cardiovascular disease risk factors, including reduced LDL cholesterol and improved insulin sensitivity, as well as greater body fat loss on energy-restricted diets.

Molecular studies indicate that physiological hyperglycemia induces overproduction of superoxide by the mitochondrial electron-transport chain, resulting in inflammatory responses and endothelial dysfunction.
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Reversing type 2 diabetes ...
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Effect of a low-carbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes. Ann Intern Med. 2005 Mar 15;142(6):403-11.

INTERVENTION: Usual diets for 7 days followed by a low-carbohydrate diet for 14 days.

RESULTS: On the low-carbohydrate diet, mean energy intake decreased from 3111 kcal/d to 2164 kcal/d. The mean energy deficit of 1027 kcal/d (median, 737 kcal/d) completely accounted for the weight loss of 1.65 kg in 14 days (median, 1.34 kg in 14 days).

Mean 24-hour plasma profiles of glucose levels normalized, mean hemoglobin A1c decreased from 7.3% to 6.8%, and insulin sensitivity improved by approximately 75%. Mean plasma triglyceride and cholesterol levels decreased (change, -35% and -10%, respectively).
=================

Biochemical explanation (of how glycemic load can cause diabetes) ...
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Association between dietary factors and plasma adiponectin concentrations in men. Am J Clin Nutr. 2005 Apr;81(4):780-6.

BACKGROUND: Adiponectin, an adipocyte-derived peptide, improves insulin sensitivity, has antiinflammatory and antiatherogenic effects, and is associated with a lower risk of ischemic heart disease (IHD) and type 2 diabetes.

OBJECTIVE: Our objective was to examine cross-sectionally the association between dietary factors and plasma adiponectin in men.

RESULTS: After multivariable adjustment, adiponectin was significantly inversely related to glycemic load (-1.3 mg/L per 1-SD increase; P = 0.02) and tended to be positively associated with total fat intake (0.7 mg/L per 0.5% of energy from fat instead of carbohydrates; P = 0.06).
=================

Successful long-term Glycemic Load intervention ...
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Comparison between a low glycemic load diet and a Canada Food Guide diet in cardiac rehabilitation patients in Ontario. Can J Cardiol. 2005 May 1;21(6):489-94.

METHODS: One hundred twenty patients who were advised to follow a low glycemic load diet were evaluated and compared with 1434 patients who were advised to follow the principles of Canada's Food Guide to Healthy Eating for People Four Years and Over as part of the Ontario Cardiac Rehabilitation Pilot Project.

RESULTS: Patients on the low glycemic load diet lost more weight at six months (2.8 kg loss versus 0.2 kg gain, P < 0.0001), had a greater reduction in abdominal obesity (2.9 cm versus 0.4 cm, P < 0.0001), and had a greater improvement in high density lipoprotein cholesterol (0.14 mmol/L versus 0.02 mmol/L, P < 0.0001), triglycerides (-0.44 mmol/L versus -0.08 mmol/L, P < 0.0001) and glycemic control (fasting glucose -0.94 mmol/L versus 0.91 mmol/L, P = 0.0019).

CONCLUSIONS: Implementation of a low glycemic load diet was associated with substantial and sustained improvements in abdominal obesity, cholesterol and glycemic control.
=================

Fat rats with blood sugar issues (from too low of a ratio of protein-to-carbs) ...
=================
Increasing the protein:carbohydrate ratio in a high-fat diet delays the development of adiposity and improves glucose homeostasis in mice. J Nutr. 2005 Aug;135(8):1854-8.

The aim of this study, therefore, was to investigate the effects of high-fat, isoenergetic diets with different protein:carbohydrate (CHO) ratios on obesity, energy metabolism, and glucose homeostasis in mice.

Male adult C57BL/6J mice consumed ad libitum for 10 wk a control diet (41:42:17 ratio of CHO:protein:fat, 15.5 kJ/g) or 2 different high-fat diets: high carbohydrate (HC; 41:16:43, 17.7 kJ/g) or low carbohydrate (LC; 11:45:44, 17.5 kJ/g).

Body weight and fat gains were rapid and were greater in HC mice than in other groups due to an initial pronounced hyperphagia and subsequent passive overconsumption.

Blood glucose was lower and insulin sensitivity greater in LC mice than in HC mice.

However, glucose homeostasis was improved in LC mice, indicating that a combination of high fat and high CHO is responsible for the development of metabolic syndrome-related traits in mice.
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But what about the big people? ...
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Lasting improvement of hyperglycaemia and bodyweight: low-carbohydrate diet in type 2 diabetes. A brief report. Ups J Med Sci. 2005;110(2):179-83.

A group of 16 obese patients with type 2 diabetes was advised on a low-carbohydrate diet, 1800 kcal for men and 1600 kcal for women, distributed as 20% carbohydrates, 30% protein and 50% fat.

Fifteen obese diabetes patients on a high-carbohydrate diet were control group. Their diet, 1600-1800 kcal for men and 1400-1600 kcal for women, consisted of approximately 60% carbohydrates, 15% protein and 25% fat.

After 6 months a marked reduction in bodyweight of patients in the low-carbohydrate diet group was observed, and this remained one year later.

After 6 months the mean changes in the low-carbohydrate group and the control group respectively were (+/-SD): fasting blood glucose (f-BG): -3.4 +/- 2.9 and -0.6 +/- 2.9 mmol/l; HBA1c: -1.4 +/- 1.1% and -0.6 +/- 1.4%; Body Weight: -11.4 +/- 4 kg and -1.8 +/- 3.8 kg; BMI: -4.1 +/- 1.3 kg/m_ and -0.7 +/- 1.3 kg/m_.

Large changes in blood glucose levels were seen immediately. A low-carbohydrate diet is an effective tool in the treatment of obese patients with type 2 diabetes.
=================

It's tough to counter this evidence. No, that would require either a heap of evidence, or a heap of evasion.

Ed
[the man who healed America's mind]

;-)

Post 39

Thursday, March 9, 2006 - 11:46am