Electronic Engineers and Dietary Advice

Do you remember DiseaseProof’s week-long examination of The Atkins Diet? In it Dr. Fuhrman discusses the risks and misinformation associated with high-protein diets. In case you missed it, here are the five posts:

Now, why do I bring this up again? Well as you can imagine it more than miffed many of the low-carb loonies out there. One in particular was Barry Groves, PhD. Who is he? To quote Dr. Fuhrman, Barry Groves is “an electronic engineer and honorary board member of the Weston Price Foundation.” Mr. Groves was so flustered by Dr. Fuhrman’s opinion of high-protein diets that he actually made a few comments, that later spawned a couple of posts. Here they are:

The last post in particular has proved quite popular. Now even though it’s many months old and buried deep in the archives it’s still good for an occasional comment. But most of the comments are nothing more than lemming-like meat mongering or Fuhrman bashing. Like this:

Why does saturated fat increase cholesterol? Why the addition of a few hydrogen atoms suddenly makes fat more likely to be turned into cholesterol? what ISOLATED, OBJECTIVE, REPEATABLE evidence do you have that saturated fat from healthy sources increases cholesterol? im not either for your argument or against it, its just i have searched the internet for PROOF of the health harming effects of saturated fat and found none.

Epidemiological evidence is nothing like enough! groves has plenty of that in his favour and you seem to have a small amount in yours, but neither is any form of proof. You can correlate sesame seeds with cancer but only because there sprinkled upon most burgers.

You should not post YOUR OPINION as though it is scientific fact, many real scientists disagree, so it seems to me either you PROOVE IT or ZIP IT.

So as you can imagine I just approve comments like this and pay them no mind. But that doesn’t mean the occasional negative comment or dissenting opinion is just automatically ignored. Actually, a well supported counterclaim is always welcome here on DiseaseProof. Check out this one from last week:

Most Importantly we should remember that no randomised controlled Clinical Trial has ever shown any reduction at all in Coronary heart Disease mortality or overall mortality from replacing animal fats with polyunsaturated vegetable fats.

In fact, just the opposite persons randomised to polyunsaturated fat had significant increases in Coronary Heart Disease mortality rates.
Are you familiar with the research Dr. Fuhrman?

There are 18 Clinical Dietary Intervention Trials and 26 prospectiuve Trials to date on the saturated fat/Coronary Heart Disease issue.

Here are all 18 Clinical and you can look them up at a Medical University Library to confirm it everyone.

*Sydney Diet Heart Study
*National Diet heart Study
*Los Angeles Veterans Administration Study
*Ball et al
*Minnesota Survey
*Lyon Diet Heart Study
*Women's Health Initiative
*Bierenbaum et al
*Anti Coronary Club
*Medical Research Council
*Hood et al
*Finnish Mental Hospital Stusy
*Medical research Council
*Rose etal
*Oslo Diet Heart Study

Clearly when you look these up you will see the research does not support the anti-cholesterol/anti-saturated fat paradigm.

Okay, now as I’ve said many times before, I’m not the expert. So when DiseaseProof receives a comment like this, I pass it on to the man. And here’s what Dr. Fuhrman say—it’s thorough to say the least:

I am familiar with the research, but there are lots more than that. I have made an effort to review every study on this subject in the last 20 years and through a comprehensive view of all the literature, the message is clear. I realize that there are people out there that deny the link between a diet rich in animal products and heart disease, diet and cancer and diet and any disease. The internet has become a forum for all different type of individuals to express their alternative beliefs, and the occasional disagreeing comments here serve a good purpose because by addressing them it helps the informed health seeker improve their view of the issues and get a better handle of the complexities of human nutrition. It is only that I am so busy working that makes the length of these responses somewhat limited and that to get the whole view it would help to first read Eat to Live and then review the posts here on this subject that have been already posted before reading this one.

I think if this commenter was already familiar with my body of work and not just commenting on one issue in a vacuum he may have already understood my answer here. Also, obviously, this is a complicated subject, but I have addressed the complexities before on this blog and in my recent newsletter addressing the poor science promoted by the Weston Price crowd and those denying that the amount and the type of animal products in one’s diet does matter when it comes to disease risk. More explanation can’t hurt though and we can review the reasons for the inconsistency in the scientific studies.

Eating less animal products and avoiding trans fat and in their place, utilizing more fruits and vegetables, beans and nuts is a goal of those seeking to reduce their risk of both heart disease and cancer. The evidence regarding these guidelines is overwhelming and I have referenced over 1500 scientific references in Eat to Live. What makes my dietary advice somewhat unique is that I insist that increasing the micronutrient density of food is an important component of a good diet and that foods that are naturally rich in vitamins and minerals are also rich in thousands of phytochemicals that are a critical (but largely ignored and unmeasured) link to good health. Since 90 percent of calories consumed in America is either animal products or processed foods, neither which contain antioxidants and phytochemicals, we suffer the medical tragedies as a result of this nutritional folly. It is the total micronutrient and phytochemical density of the diet which is more important in disease-prevention than moderating fat intake. The standard modern diet is disease-promoting and just decreasing or exchanging the type of fat can’t change its pitiful level of protective nutrients. I repeat, micronutrient density and variety overwhelms saturated fat (lowering) as a disease protector. If interested, as it will help you understand this, check out the library on DrFuhrman.com. There you can view a chart of nutrient per calorie density of selected foods.

I also teach that the saturated fat content of the animal products chosen to include in one’s diet does also make a difference when it comes to health science and promoting optimal health; not just for heart disease, but for cancer reduction too. Animal fats are more risky than vegetable fats, but they both promote disease if eaten in excess and the fact that cheese has much more saturated fat than fish and fowl, makes it a more risky food to include in one’s diet in any substantial amount. That does not mean I advocate eating vegetable oils and consider them health foods. I am not a promoter of processed oils as they dilute the nutrient density of our diet and are a high calorie, low nutrient food. Saturated fat does not become good because trans fat and some processed oils are bad. Polyunsaturated oils are processed foods, consumed in a rancid state, with little or no fiber, micronutrients, antioxidants or phytochemicals. In no way do I agree with Walter Willet and other highly esteemed names in the field of nutritional science who think that substituting polyunsaturated oils in place of saturated fats is the answer for optimal health. Oil is too fattening a food to be promoted has health food and I thinks Willet’s message to put olive oil and other polyunsaturated and monounsaturated oil at the base of a nutrition pyramid is ridiculous and most likely reflects his desire to commercially appeal to America’s food preferences. Instead, I recommend most of our fat intake come in the whole food form from flax seeds, walnuts, sunflower seeds, avocados, sesame seeds and other foods that are not only rich in healthy fats, but also contain antioxidants, lignans, flavonoids and other protective compounds (and I make delicious salad dressings from these whole-food plant fats).

When we consider these complicated issues we must be familiar with hundreds and in some cases thousands of research articles to understand the complexities of human nutrition. One thing that stands out in all this is that it is not one element good or bad that can explain the complicated nutritional component in disease-causation. So I would never encourage the thinking that looking at saturated fat intake alone in a diet and no other critical factors would afford us good health and protection from heart disease and cancer. Comparing one type of low nutrient diet to another does not show much, they are all bad. But I agree with the point made by some of the articles the commenter mentioned; that moderate reductions in saturated fat intake, in an elderly population, while the diet stays relatively low in high-nutrient plant foods is not likely to offer dramatic health benefits. Especially because what we do at a younger age has a more powerful effect to modulate the expression of these later life diseases compared to what we do at a later age. This is especially true with cancer, where we expect to see a 25 to 50 year lag time between cause and effect. So another element that this question and a review of all these studies indicate is that the earlier in life that dietary change is instituted more dramatic protective effects are seen and the later in life, the smaller the benefit, if any. I spend a lot of time discussing this in my book, Disease-Proof Your Child, which explained that dietary factors in childhood are the largest component of adult cancer causation.

More recent studies are accumulating that show eating more high-nutrient plant food is a more powerful intervention to prevent disease, than just reducing saturated fat alone. You can reduce cheese and butter and still be eating a crummy, low nutrient, disease-promoting diet; big deal! But the best protection from disease occurs and the most dramatic amount of disease reversal is accomplished when the diet is both low in saturated fat and high in micronutrients. This is the pattern of the dietary recommendations in Eat to Live and my other works. Eat to Live because it is written for the overweight individual is more restricted in nuts, seeds and avocados (higher fat, higher calorie plant foods) compared to Disease-Proof Your Child, which contains dietary guidelines somewhat higher in the fattier whole foods (healthy fats) geared for a general audience, not for those who are so weight-challenged.

So even though we could point to some older studies that looked at a population with a high animal product intake and then compared it to one that was still high in animal products but somewhat lower in saturated fat and added oils to it, to show an unclear differences in outcome is not surprising. Especially when both studied diets are still rich in processed foods and animal product, and especially when the subjects are older and not followed for enough years to see the differences or when both the size of the study, the amount of dietary change, and the number of years studied make the difference in “relative risk” insignificant. So contrary to the commenter’s assertion most of the studies mentioned show insignificant and inconsistent mortality differences. When you read the whole study, you can usually understand why it found the outcome it did and the better quality studies explain the inconsistencies better. And you have to look at the nutritional quality of the whole diet studied to predict the outcomes not merely one of the many variables that give a diet its disease promoting or health promoting properties.

Let’s look at some of the most recent studies (click “Permalink” or “Continue Reading”) and see what they really say. Oh, and for other readers who want to post references to support their views, like this commenter did, please include the complete reference so others can easily look it up and check the facts.

Of course some people are not interested in science or logic, to them nutrition is based on emotion and what they want to believe and what they want to eat and no matter what I say or the research says won’t change their fixed views.

Don’t forget, click Permalink or Continue Reading to check out those studies Dr. Fuhrman mentioned—there’s a bunch of them!


The effect of a plant-based diet on plasma lipids in hypercholesterolemic adults: a randomized trial. Ann Intern Med. 2005; 142(9):725-33. Gardner CD ; Coulston A ; Chatterjee L ; Rigby A ; Spiller G ; Farquhar JW

This recent study showed that when two diets have the same amount of fat and saturated fat, it is the one with the higher amount of high nutrient plant material that gives the best results for cholesterol lowering and other measurable disease-risk parameters.

Here is the conclusion of the abstract mentioned it has been copied here without modification:

CONCLUSIONS: Previous national dietary guidelines primarily emphasized avoiding saturated fat and cholesterol; as a result, the guidelines probably underestimated the potential LDL cholesterol-lowering effect of diet. In this study, emphasis on including nutrient-dense plant-based foods, consistent with recently revised national guidelines, increased the total and LDL cholesterol-lowering effect of a low-fat diet.

The combination of high fruit and vegetable and low saturated fat intakes is more protective against mortality in aging men than is either alone: the Baltimore Longitudinal Study of Aging. J Nutr. 2005; 135(3):556-61. Tucker KL ; Hallfrisch J ; Qiao N ; Muller D ; Andres R ; Fleg JL ;

Saturated fat (SF) intake contributes to the risk of coronary heart disease (CHD) mortality. Recently, the protective effects of fruit and vegetable (FV) intake on both CHD and all-cause mortality were documented. However, individuals consuming more FV may be displacing higher-fat foods. Therefore, we investigated the individual and combined effects of FV and SF consumption on total and CHD mortality among 501 initially healthy men in the Baltimore Longitudinal Study of Aging (BLSA). Over a mean 18 y of follow-up, 7-d diet records were taken at 1-7 visits. Cause of death was ascertained from death certificates, hospital records, and autopsy data. After adjustment for age, total energy intake, BMI, smoking, alcohol use, dietary supplements, and physical activity score, FV and SF intakes were individually associated with lower all-cause and CHD mortality (P < 0.05). When both FV and SF were included in the same model, associations of each were attenuated with CHD mortality, and no longer significant for all-cause mortality. Men consuming the combination of > or =5 servings of FV/d and < or =12% energy from SF were 31% less likely to die of any cause (P < 0.05), and 76% less likely to die from CHD (P < 0.001), relative to those consuming < 5 FV and >12% SF. Men consuming either low SF or high FV, but not both, did not have a significantly lower risk of total mortality; but did have 64-67% lower risk of CHD mortality (P < 0.05) relative to those doing neither. These results confirm the protective effects of low SF and high FV intake against CHD mortality. In addition, they extend these findings by demonstrating that the combination of both behaviors is more protective than either alone, suggesting that their beneficial effects are mediated by different mechanisms.
Effect of diet intervention on long-term mortality in healthy middle-aged men with combined hyperlipidaemia. J Intern Med. 2004; 255(1):68-73. Hjerkinn EM ; Sandvik L ; Hjermann I ; Arnesen H

Initially healthy men in the 40-49 age range were randomized to two groups and one group was counseled for five years to reduce saturated fat in their diet and eat a more heart healthy diet. In the 24 year period the intervention group had half as many deaths. The conclusion stated:

CONCLUSION: This study indicates that the investigated 5-year diet intervention significantly reduces late mortality in healthy middle-aged men with combined hyperlipidaemia.

A prospective study of variety of healthy foods and mortality in women.
Int J Epidemiol. 2002; 31(4):847-54. Michels KB ; Wolk A

59,000 women were studied and those consuming healthier foods including a variety of fruits and vegetables and less animal products had a 42 percent lower all-cause mortality.

CONCLUSIONS: A healthy diet can affect longevity. It appears more important to increase the number of healthy foods regularly consumed than to reduce the number of less healthy foods regularly consumed.

Dietary primary prevention of cardiac ischemic diseases. Arch Mal Coeur Vaiss. 2003; 96 Spec No 6:21-5. Chanu B.

Population studies have shown that heart disease is more frequent in countries where the inhabitants have diets rich in saturated fats and in cholesterol, and where blood cholesterol levels are raised. The epidemiological data from large prospective studies have shown that total cholesterol is positively correlated with coronary risk. Primary prevention dietetic trials have often been disappointing, probably due to a drop in cholesterol which is too modest, insufficient study size and duration, and perhaps also because they concerned low risk subjects. A meta-analysis of 27 primary and secondary prevention dietetic studies produced evidence of a reduction in morbidity, principally when the studies lasting less than 2 years were not taken into account. In this meta-analysis the drop in cholesterol was correlated with a reduction in clinical events. The benefit of a modified fat diet in primary prevention is therefore potentially significant if it is maintained for a sufficient length of time. The very positive results of the American national program of nutritional intervention, which has had an undeniable impact on the prevalence of lipid disorders in the general population and secondarily on coronary mortality, has been more effective than drugs in reducing cardiovascular mortality.
Cholesterol, coronary heart disease and stroke: a review of published evidence from observational studies and randomized controlled trials. Semin Vasc Med. 2002; 2(3):315-23. Huxley R ; Lewington S ; Clarke R

In observational epidemiologic studies, lower blood cholesterol is associated with a reduced risk from coronary heart disease (CHD) throughout the normal range of cholesterol values observed in most Western populations. There is a continuous positive relationship between CHD risk and blood cholesterol down to at least 3 to 4 mmol/l, with no threshold below which a lower cholesterol is not associated with a lower risk. Observational studies suggest that a prolonged difference in total cholesterol of about 1 mmol/l is associated with one-third less CHD deaths in middle age. Evidence from large-scale cholesterol lowering trials in patients at high-risk of CHD have demonstrated that much of the epidemiologically predicted difference in CHD risk associated with differences in cholesterol was achieved within a few years of treatment. Moreover, these trials have demonstrated that such therapy was not associated with increased non-CHD mortality. Total cholesterol is transported in blood as low-density lipoprotein cholesterol or LDL cholesterol (about 70%) and as high density lipoprotein cholesterol or HDL cholesterol (about 30%). Since these two cholesterol fractions have opposing effects on vascular risk, a 1 mmol/l reduction in LDL cholesterol is likely to be associated with 40 to 50% lower CHD risk. The size of the absolute reduction in CHD produced by lowering total and LDL cholesterol is determined by an individual's overall risk rather than their initial cholesterol level. Consequently, the benefits of drug treatment to lower LDL cholesterol are greater in those at higher absolute risk of CHD rather than at high cholesterol levels. Dietary saturated fat is the chief determinant of total and LDL cholesterol levels. Replacing 60% of the intake of saturated fat by other fats and reducing the intake of dietary cholesterol could reduce blood total cholesterol levels by about 0.8 mmol/l (that is by 10 to 15%), with four fifths of this reduction being in LDL cholesterol.

The effect of replacing dietary saturated fat with polyunsaturated or monounsaturated fat on plasma lipids in free-living young adults. Eur J Clin Nutr. 2001; 55(10):908-15.

Hodson L ; Skeaff CM ; Chisholm WA

Two randomized controlled trial showing that when saturated fat foods were restricted in favor of vegetable polyunsaturated or monounsaturated fats, lowered blood cholesterol by about 20 percent (LDL by 22 percent). Authors conclusion:

Replacing saturated fat with either n-6 polyunsaturated or monounsaturated fat is equally efficacious at reducing the total to high density lipoprotein cholesterol ratio.

Relation between fat intake and mortality: an ecological analysis in Belgium.
Eur J Cancer Prev. 1997; 6(4):374-81. Staessen L ; De Bacquer D ; De Henauw S ; De Backer G ; Van Peteghem C.

A representative sample of the Belgian population, aged 25-74 years, was interviewed between 1980 and 1985. Age-, sex- and district-specific energy-adjusted averages of macronutrient intakes were compared with mortality rates from 1988-90, with special emphasis on the association between fat intake and cancer mortality. In multivariate analyses, significant positive associations were found between all-causes mortality and saturated fat intake in men, and between all-causes mortality and the ratio of n-3 to n-6 fatty acids in men. In women, breast cancer mortality was associated with saturated and monounsaturated fat intake.

Saturated fat, vitamin C and smoking predict long-term population all-cause mortality rates in the Seven Countries Study. Int J Epidemiol. 2000; 29(2):260-5. Kromhout D ; Bloemberg B ; Feskens E ; Menotti A ; Nissinen A

Baseline surveys were carried out between 1958 and 1964 on 12,763 middle-aged men constituting 16 cohorts in seven countries. In 1987/88 equivalent food composites representing the average food intake of each cohort at baseline were collected and chemically analyzed in one central laboratory. During 25 years of follow-up 5973 men died and age-adjusted population mortality rates were calculated for each cohort. RESULTS: Multivariate linear regression analyses showed that the population intake of saturated fat and the prevalence of smoking were positively associated with population all-cause mortality rates. Population vitamin C intake was inversely associated with all-cause mortality.

At the population level saturated fat, vitamin C and cigarette smoking are important determinants of all-cause mortality.

Dietary fat intake and risk of coronary heart disease: the Strong Heart Study. Am J Clin Nutr. 2006; 84(4):894-902. Xu J ; Eilat-Adar S ; Loria C ; Goldbourt U ; Howard BV ; Fabsitz RR ; Zephier EM ; Mattil C ; Lee ET.

The results of previous studies on the association between dietary fat intake and coronary heart disease (CHD) incidence are inconsistent. A total of 2938 participants aged 47-79 y and free of CHD at the second examination (1993-1995) were examined and followed for CHD, nonfatal CHD, and fatal CHD events to 31 December 2002. Participants were followed for a mean (+/-SD) of 7.2 +/- 2.3 y. During follow-up, 436 incident CHD cases (298 nonfatal CHD and 138 fatal CHD events) were ascertained. Participants aged 47-59 y in the highest quartile of intake of total fat, saturated fatty acids, or monounsaturated fatty acids had higher CHD mortality than did those in the lowest quartile Total fat, saturated fatty acid, and monounsaturated fatty acid intake were strong predictors of CHD mortality in American Indians aged 47-59 y, independent of other established CHD risk factors. It may be prudent for American Indians to reduce their fat intake early in life to reduce the risk of dying from CHD.

Diet and coronary heart disease: clinical trials. Curr Atheroscler Rep. 2000; 2(6):487-93. Brousseau ME ; Schaefer EJ

Dietary intervention trials using coronary heart disease (CHD) mortality and morbidity as endpoints have demonstrated that restriction of dietary total and saturated fat or replacement of the latter with polyunsaturated fatty acids (PUFAs), in particular n-3 PUFAs, is of great benefit with respect to CHD risk. This is likewise the case for intervention trials using angiographic endpoints, with many studies showing that such diets not only retard progression of coronary atherosclerosis but can cause regression as well.

Dietary pattern and 20 year mortality in elderly men in Finland, Italy, and The Netherlands: longitudinal cohort study. BMJ. 1997; 315(7099):13-7 (ISSN: 0959-8138)

Huijbregts P ; Feskens E ; Räsänen L ; Fidanza F ; Nissinen A ; Menotti A ; Kromhout D

Population based random sample of 3045 men aged 50-70 years in 1970. RESULTS: Dietary intake varied greatly in 1970 between the three countries. In Finland and the Netherlands the intake of saturated fatty acids and cholesterol was high and the intake of alcohol was low; in Italy the opposite was observed. In total 1796 men (59%) died during 20 years of follow up. The healthy diet indicator was inversely associated with mortality (P for trend < 0.05). After adjustment for age, smoking, and alcohol consumption, the relative risk in the group with the healthiest diet indicator compared with the group with the least healthy was 0.87 (95% confidence interval 0.77 to 0.98). Estimated relative risks were essentially similar within each country. CONCLUSIONS: Dietary intake of men aged 50-70 is associated with a 20 year, all cause mortality in different cultures. The healthy diet indicator is useful in evaluating the relation of mortality to dietary patterns.

The Oxford Vegetarian Study: an overview. Am J Clin Nutr. 1999; 70(3 Suppl):525S-531S (ISSN: 0002-9165) Appleby PN ; Thorogood M ; Mann JI ; Key TJ

The Oxford Vegetarian Study is a prospective study of 6000 vegetarians and 5000 nonvegetarian control subjects recruited in the United Kingdom between 1980 and 1984. Cross-sectional analyses of study data showed that vegans had lower total- and LDL-cholesterol concentrations than did meat eaters; vegetarians and fish eaters had intermediate and similar values. Meat and cheese consumption were positively associated, and dietary fiber intake was inversely associated, with total-cholesterol concentration in both men and women. After 12 y of follow-up, all-cause mortality in the whole cohort was roughly half that in the population of England and Wales (standardized mortality ratio, 0.46; 95% CI, 0.42, 0.51). After adjusting for smoking, body mass index, and social class, death rates were lower in non-meat-eaters than in meat eaters for each of the mortality endpoints studied [relative risks and 95% CIs: 0.80 (0. 65, 0.99) for all causes of death, 0.72 (0.47, 1.10) for ischemic heart disease, and 0.61 (0.44, 0.84) for all malignant neoplasms]. Mortality from ischemic heart disease was also positively associated with estimated intakes of total animal fat, saturated animal fat, and dietary cholesterol. Other analyses showed that non-meat-eaters had only half the risk of meat eaters of requiring an emergency appendectomy, and that vegans in Britain may be at risk for iodine deficiency. Thus, the health of vegetarians in this study is generally good and compares favorably with that of the nonvegetarian control subjects. Larger studies are needed to examine rates of specific cancers and other diseases among vegetarians.

Dietary fatty acids and coronary heart disease. Eur J Med Res. 2003; 8(8):321-4. Wolfram G.

Epidemiological studies have confirmed a strong association between fat intake, especially saturated and trans fatty acids, plasma cholesterol levels and rate of coronary heart disease (CHD) mortality. Meanwhile it is clear, that early atherosclerosis is largely preventable by modifying nutritional behaviour and lifestyle. There is clear evidence that a diet moderate in total fat (25-35 % energy) is superior to extremes in dietary fat. Because fat is energy dense moderation in fat intake is also essential for weight control. Saturated fatty acids are very potent in increasing LDL-cholesterol concentration in plasma a dangerous risk factor for early CHD. Unsaturated fatty acids have numerous beneficial health effects. The results of prospective cohort studies fit well to the experimental experience of the antihypercholesterolemic action of Omega-6 fatty acids and the antithrombotic, vasodilatory and antiarrhythmic properties of Omega-3 fatty acids, while the optimistic rating of Omega-9 fatty acids is less supported by epidemiologic studies. The results of prospective cohort studies are confirmed by intervention trials revealing that saturated fatty acids enhance early development of CHD whereas polyunsaturated fatty acids, especially of the Omega-3 type, significantly preserve from CHD. In context with a prudent diet pattern favourable dietary fatty acid composition offers the best chance for a reduced risk of CHD.

Dietary fats, carbohydrates and vascular disease: Sri Lankan perspectives. Atherosclerosis. 2003; 171(2):157-61. Abeywardena MY

The recent estimates for mortality from cardio and cerebrovascular diseases (CVD) for Sri Lanka--524 deaths per 100,000--is higher than that observed in many Western economies. However, neither an excessive total fat intake nor an increase in the more traditional plasma lipid markers, total and LDL cholesterol (LDL-c) levels may fully explain the increased vulnerability to CVD in this population. The average total fat intake of Sri Lankans is 25 percent of total energy (en%) and the reported total and LDL-c values are 4.9 and 2.5 mmol/l, respectively. With regard to the type of dietary fatty acids, the ratio of saturated/polyunsaturated fatty acids (PUFAs) in the average Sri Lankan diet is 9/1 as compared with the current recommended ratio of <1/1. In spite of an adequate total fat intake (25 en%), the relatively low intake of PUFAs in association with a high carbohydrate diet (65 en%), appear to be resulting in similar metabolic outcomes to those of very low fat diets (VLFD, < 15 en% from fat), as reflected by high triglycerides and low HDL levels. Metabolic abnormalities including elevated postprandial hyperlipidemia, more atherogenic lipoprotein particles, hyperglycemia with resultant hyperinsulinemia and increased oxidative stress are likely to be more relevant in such settings. The application of novel biomarkers for example, lipoprotein measurements in the postprandial state, LDL particle size, estimates of endothelial dysfunction, soluble markers of inflammation and coagulability status may provide further insight into cardiovascular disease states in populations where the dietary matrix represents high intakes of highly digestible carbohydrates and saturated fat.

Dietary intake and the risk of coronary heart disease among the coconut-consuming Minangkabau in West Sumatra, Indonesia. Asia Pac J Clin Nutr. 2004; 13(4):377-84. Lipoeto NI ; Agus Z ; Oenzil F ; Wahlqvist M ; Wattanapenpaiboon N.

Several nutrition and non-nutritional pathways are recognized in the development and occurrence of cardiovascular disease. In many populations, high intakes of saturated fat are associated with elevated serum cholesterol concentrations and increased coronary heart disease (CHD) mortality. However, several studies report that hyperlipidaemia and heart diseases are not common among populations who consume coconut, a source of saturated fat. A case-control study was conducted among the Minangkabau known to be high coconut consumers to examine the difference in food patterns and risk of coronary heart disease (CHD) between the coronary cases and their gender- and age-matched apparently healthy counterparts serving as controls. Eligible subjects with CHD were identified through the co-operation of five participating hospitals located in Padang and Bukittinggi in West Sumatra, Indonesia. A total of 93 eligible cases (62 men and 31 women) in the Case group and 189 subjects (113 men and 76 women) in the Control group were recruited. Information on the intakes of individual foods and dishes over the preceding 12 months was obtained using a semi-quantitative food frequency questionnaire. The Case groups had significantly higher intakes of meats, eggs, sugar, tea, coffee and fruits, but lower intakes of soy products, rice and cereals compared to the controls. Coconut consumption as flesh or milk was not different between cases and controls. The cases had significantly higher intakes of protein and cholesterol, but lower intake of carbohydrate. Similar intakes of saturated and unsaturated fatty acids between the cases and controls indicated that the consumption of total fat or saturated fat, including that from coconut, was not a predictor for CHD in this food culture. However, the intakes of animal foods, total protein, dietary cholesterol and less plant derived carbohydrates were predictors of CHD.

Types of dietary fat and risk of coronary heart disease: a critical review. J Am Coll Nutr. 2001; 20(1):5-19. Hu FB ; Manson JE ; Willett WC

During the past several decades, reduction in fat intake has been the main focus of national dietary recommendations to decrease risk of coronary heart disease (CHD). Several lines of evidence. however, have indicated that types of fat have a more important role in determining risk of CHD than total amount of fat in the diet. Metabolic studies have long established that the type of fat, but not total amount of fat, predicts serum cholesterol levels. In addition, results from epidemiologic studies and controlled clinical trials have indicated that replacing saturated fat with unsaturated fat is more effective in lowering risk of CHD than simply reducing total fat consumption. Moreover, prospective cohort studies and secondary prevention trials have provided strong evidence that an increasing intake of n-3 fatty acids from fish or plant sources substantially lowers risk of cardiovascular mortality. In this article, we review evidence from epidemiologic studies and dietary intervention trials addressing the relationship between dietary fat intake and risk of CHD, with a particular emphasis on different major types of fat, n-3 fatty acids and the optimal balance between n-3 and n-6 fatty acids. We also discuss the implications of the available evidence in the context of current dietary recommendations

Trackbacks (0) Links to blogs that reference this article Trackback URL
Comments (7) Read through and enter the discussion with the form at the end
mrfritznyc - December 27, 2006 10:42 AM

Happy Holidays, I just wanted to tell you that in my case, eating a low carb diet for five straight years has only been beneficial for me. I've lost weight, my asthma went away, my triglycerides are very low, my HDL is high, my LDL, while you might consider it high, is almost all the large fluffy type A - considered beneficial. I also had a CT scan done, because my doc. was worried about my LDL, my results were a Agaston score of ZERO. Meaning absolutely no plaque.

So, sorry, when considering my own experience, and especially when considering the evolutionalry evidence, your contention that sat. fat is dangerous seems a bit misguided.

Reggie - December 27, 2006 11:14 AM

Ha Ha Ha! Misguided? MrFritznyc you are calling all of the research supporting dr. Fuhrman's position misguided when you are basing the merits of low carb diets on just one personal experience. You sir are misguided.

mrfritznyc - December 27, 2006 11:54 AM

reggie, i refer you back to my post, where I said "and especially when considering the evolutionalry evidence"... let me explain - I beieve the anthropoligists who tell us we evolved to what we are now in large part because we started eating animal protein and continued to eat animal protein for thousands and thousands of years. To take the position that animal protein is now somehow bad for us seems to me to be a bit, well, er, a bit of a challenge, logically speaking...

never mind my own personal experience, you should consider that of thousands of low carbers who post at various forums and report similar results. When you cut down on the carbs, a diet that is rich in sat. fat always improves your cholestoral. And, by the way, it improves a wide array of medical conditions.

row - December 27, 2006 2:26 PM

happy holidays to you to mrfritnyc!
since you did make some comments about how well your doing on a low carb diet and how your asthma improved. I thought others might like to see how your doing, this was taken from "livin'La Vida Low-Carb" web site. In your own words, written just a few days ago.

Drinking lots of alcohol and taking drugs for your asthma! I like the commment about most low carb people not meeting their goals, which is different than the one you posted here at diseaseproof stating how great there are doing. your qoute,
[never mind my own personal experience, you should consider that of thousands of low carbers who post at various forums and report similar results. When you cut down on the carbs, a diet that is rich in sat. fat always improves your cholestoral. And, by the way, it improves a wide array of medical conditions.

Cholestrol from the a low-carb stand point is a myth, high numbers don't mean a thing. Low-carb people don't worry about cholestrol.
At 12/13/2006 10:31 AM, mrfritznyc said

here's my version of your list, it's only slightly different:

1. Eat low-carb foods.
2. Eat only enough to satisfy my hunger.
3. Lift weights twice a week ("Slow Burn" style).
4. Do it for the rest of my life.
At 12/14/2006 6:28 PM, mrfritznyc said

is scotch a medicine? if so, I take plenty! beer too! no other medicines to, except claratin for my allergies.

i eat loads of high quality fat and protein, I am a very good customer at www.uswellnessmeats.com, my source for tender succulent grass-fed ribeyes..

according to a BMR calculator I found today, my BMR is about 1800 calories per day. I am 50 years old, just under 6', weight 189. I suspect my BMR is a little bit lower, actually, but that sounds about right. When I was eating all I wanted, low carb style, I was eating about 2200-2400 - which explains why I stopped losing weight - after dropping 30 or so pounds.

it's not rocket science. when I trim my calories back to 1500 or 1600ish, I start losing weight. duh!

Of course,I'd lose more if I skipped the scotch, but I'm not that desperate!

I suppose it's possible that I might have candida, but I doubt it
At 12/15/2006 11:00 AM, mrfritznyc said
you may be right about the asthma and low carbing, I havent had an asthma flare up since I started 4 and 1/2 years ago.

however, I cant believe a claratin pill has enough of anything that would hinder my weight loss. you know, once in awhile I'll eat some bread at a restaraunt or even a baked potato (just the pulp tho, smothered in butter and sour cream, of course!), and it has zero impact on my weight. I doubt that a tiny little pill does either.

and yes, the booze does as you say, puts ketosis on pause. Yawn. It also adds calories. But I would guess I am in ketosis at least 70 - 80 per cent of the time.

Because I lost 30 pounds while drinking pretty much the same amount as I do now, and because it's basic common sense, I am more inclined to believe the reason I stopped losing weight is because my caloric requirements dropped as I lost the initial 30 pounds. Not a big mystery here.

would I lose faster without the booze? of course. do I care? not at all!

take a look at the low carb forums and see how many long timers there are still short of their goal. that's because they believe the myth that there's something magial about low carb calories.

take a look at kimkins.com, and see how many people reach their goal with ease.

the difference is stark and should tell you something.

mrfritznyc - December 27, 2006 6:42 PM

I know you have a point there somewhere, but it's beyond me what it might be. Yes, I like to drink scotch from time to time, and yes, I do take Claratin for my allergies (not asthma, allergies). And I do happen to believe that low carb works great, up to a point. Beyond that point, most folks also need to concern themselves with calories.

I have been doing great. I lost about 40 pounds and have kept it off by doing low carb. Could I do better? Sure, I still need to lose 15 or so. Working on that now.

Not sure what any of this has to do with my contention that saturated fat is not bad for you???

mrfritznyc - December 27, 2006 6:49 PM


most anthropologists seem to agree that our brains were only able to develop at the expense of our stomachs... in order for us to have bigger brains and smaller stomachs, we needed very nutrient dense food. As in meat. there is lots of info out there on this subject, just google "expensive tissue theory" for a far better explanation I can give.
as for mother's milk, where are you getting your info? I've read that it is about 30/30/30 fat/protein/carbs, and has quite a bit of saturated fat in it too.

row - December 27, 2006 8:16 PM

Mr Fritznyc,
Losing weight is great!I had asthma at one time, I switched to a diet like dr fuhrman advocates and all my asthma and alergies completely went away, with no drugs.
In your posts it sounded like you drank a lot.I don't think drinking is a sign of good health.
You also stated that you were in ketosis 70 to 80% of the time,you also stated you were on this diet for life. you may have lost weight and you may even loose more. Being in a constant state of ketosis is not healthy, that's my point.You may think you are doing is great, I think posting what I did gives a clearer picture of where you are coming from and maybe where your going, that's all. One of us is wrong, time will tell, won't it!

Post A Comment / Question Use this form to add a comment to this entry.

Remember personal info?