DNC News


Chanukah Latkes

Jacob Schor, ND

December 1, 2006


The First Night of Chanukah comes on the Ides of December this year. That is according to the Roman calendar, which Julius Caesar bequeathed us. It was the Ides of March, which Caesar was warned to beware of in Shakespeare's play. This year's celebration will mark the 2,170th anniversary of the Maccabean rebellion when Judah and his brothers drove the Syrian armies of Antiochus from Israel . Looking back, this was a war between two cultures and a group of religious fanatics beat the super power of the day.


The holiday does not actually celebrate that military victory but instead a once upon a time miracle of improved fuel economy. Once the Syrian armies had cut and run, the Temple in Jerusalem was quickly cleaned up and rededicated. Event planners were hasty and fired up the Eternal Light without first checking fuel supplies. There was only enough holy oil to last a day; yet miraculously, it burned for eight days.


If you owned a Hummer (assuming you pay any attention to gas consumption) and it got the mileage of a Prius, you would call it a miracle too.


Because this ancient miracle involved oil, it is traditional to eat lots of oil as we celebrate Chanukah. In America , we make latkes, fried potato pancakes, in celebration. In Israel , they make jelly doughnuts. This latke tradition comes from Eastern Europe . Neither Judah the Maccabee nor Julius the Caesar saw a potato during their life times. Potatoes are a New World food. Potatoes were not grown in Europe until Spanish conquistadors brought them back from Peru in the 1500's. The people who brought us potatoes also brought Spanish Jews the Inquisition. Frying potatoes in burning hot oil might be symbolic of something else but let's not go there.



People often confess that they love their potatoes. They do this with a sense of guilt. Potatoes are no longer worshipped as the perfect food. Carb loading is out of favor. Potatoes are a vegetable in disgrace. The new health worries that people fear, hyperinsulinemia, Syndrome X, Metabolic Syndrome are all basically fancy names for people getting fat from eating too much sugar and starch. Potatoes epitomize the worst of all these worries. Glycemic index lists tell us that potatoes raise one's blood sugar as fast as white bread. Almost everyone is on one of those diets these days that frown on carbohydrates and which outlaw potatoes.


A recent lung cancer study is difficult to ignore. Writing in the journal, Lung Cancer, a group of Danish scientists with tongue twister names, answered their own question, “Can fruits and vegetables slow lung cancer?” They analyzed data from a cohort study with 57,053 participants and focused especially on the 353 participants who got lung cancer. The more fruits and vegetables these lung cancer patients ate, the longer they lived. Those who consumed the most had a risk of dying that was 20% below average. But, here's the kicker. Eating potatoes increased their chance of dying by over 50%. Potato eaters had a Hazard Ratio 153% above average. This is bad. Is there something innately bad for you in potatoes? My first thought is not that potatoes are nasty but rather this is simply a matter of room on one's plate. The more potato one eats, the less space left for other vegetables or fruits to fit on the plate. Or is this just my rationalization? Cancer death accelerated by 50% should put one off potatoes.



Maybe it's time for a new recipe. The obvious, at least in my mind, substitution for potatoes has to be cauliflower. Like potatoes, cauliflower are white. More important, from a health perspective, cauliflower is a cruciferous vegetable, related to broccoli, cabbage and Brussels sprouts. Members of this family of foods contain several chemicals which have profound cancer fighting effects. Sulforaphane is the best known of these cruciferous chemicals, made famous by researchers from John Hopkins School of Medicine when they patented broccoli sprouts. Studies show that sulforaphane stops growth in a range of cancer types including, prostate, [i] bladder, [ii] liver and colon. [iii] . An October 2006 study published in Mutation Research says sulforaphane increases the toxicity of the chemotherapy drug adriamycin against cancer cells. [iv] Where potatoes may encourage cancer to grow, cauliflower may do the opposite. A latke made from cauliflower looks just as good as a potato latke. The problem is that they don't taste as good. Trust me on this; I've been experimenting with recipes all afternoon. A decent compromise is to replace half of the potatoes with cooked and mashed cauliflower. Yet the end product tastes more like something that should be served with Indian dahl and curry rather than sour cream and applesauce. In that case perhaps we should just fry Indian style pakora, vegetables battered in chickpea flour and skip the latke business altogether.



Whether frying potato latkes or cauliflower latkes, olive oil is the perfect choice for oil.


Two thousand years ago, in the time of the Macabbees, no one was growing soy beans. Oil was pressed from olives and out of historical stubbornness, I insist on frying our Chanukah latkes in olive oil. While potatoes are sliding toward the compost pile of public opinion, olive oil gathers laurels from the scientific world for its health promoting effects. Olive oil is the foundation of all that Mediterranean diet stuff that is all the rage for researching. Eating a Mediterranean Diet is something of a modern day miracle. People who make Mediterranean-like food choices reduce all sorts of inflammatory processes, causing measurable improvement in conditions ranging from arthritis to Alzheimer's. Most of the good effect is from the olive oil. If Mediterranean diets are hot, olive oil is hotter.


A study in the September, 2006 issue of the Annals of Internal Medicine looked at varying ‘strengths' of olive oil and their effect on cardiovascular risk factors. The researchers tried three different oils whose phenolic content varied from a low of 2.7 mg/kg, to a medium grade, 164 mg/kg, and to a high phenolic content of 366 mg/kg. Two hundred healthy male volunteers were tested at 6 different hospital setting in 5 European countries. Study participants ate 25 ml of one of the oils a day for three weeks, eventually trying all three oils. The more phenols in the olive oil, the more their HDL or good cholesterol increased. At the same time, as phenolic content increased, total cholesterol decreased. [v]


Replacing potato latkes may be sacrilegious to many. There is a lot to be said for eating olive oil with potatoes. Olive acts as a stimulus helping the body process the sugar load from the potato starch better. A June 2006 study published in the Journal of Endocrinology and Metabolism confirmed earlier rodent studies. Olive oil stimulates the production of incretin hormones which in turn help regulate insulin production and blood sugar maintenance. In this study Type II diabetics ate 30 ml of olive oil before devouring a bowl of mashed potatoes. Eating the olive oil decreased the blood sugar spike the potatoes would normally have caused. [vi]


Another study, this one published in mid October, looked at the effect of different olive oils on atherosclerosis. [vii] Olive oils with a high ‘olive' content slowed atherosclerosis in mice bred to get the disease. Also related to heart disease, a July study in the Annals of Internal Medicine compared eating nuts against olive oil or against the old standby, a low fat diet. Eating either nuts or olive oil produced superior results compared to following the, now out of vogue, low fat diet. [viii] While we may question if we should eat potatoes, there is no question about olive oil, the more, the better.



This prompts me to write a few notes on how to make good potato pancakes. Chanukah is a celebration of a miracle and a good latke itself should bring happiness. Some of the latkes I have sampled in recent years should count as penance. The biggest mistake in cooking latkes is being stingy with the oil. The idea is not to lightly grease the pan to prevent the latke from sticking. The idea is almost to deep-fry the thing. Cooking with inadequate oil produces a greasy, soggy undercooked, actually half-raw, potato pancake. Using adequate oil delivers a crisp, light, fully cooked, delightfully flavored morsel. Without enough oil, the potato batter cools the oil; batter cooked at a low temperature soaks up oil like blotter paper and the lower temperatures aren't sufficient to cook the potato. Good hot oil, stays hot, the batter crisps quickly, sealing the oil out. Moisture in the batter quickly turns to steam pushing the oil outward and warding off sogginess.


There's another trick to making a good latke. Rid the potatoes of extra moisture by salting them. As you grate the potatoes and onions, sprinkle them lightly with kosher salt. Toss the grated potatoes into a colander and let them sit in the sink for a couple of minutes. Squeeze out all the water you can by using your hands and squishing the potatoes before moving the stuff into a bowl and adding the eggs and matzo meal.


Potatoes discolor quickly when exposed to oxygen and take on a gross brownish gray color. Once you peel the potatoes, keep them covered with water until you grate them. Mixing grated onions with the grated potatoes somehow stops them from turning brownish yucky as they sit. Does this really work? All the grandmothers say it does.


Don't be stingy with eggs either. They don't raise your cholesterol like we once thought. Add enough eggs so the mixture looks soft, like cake batter and then add matzah meal. I guess I add about 1 Tablespoon of meal per egg


Olive oil is not, admittedly perfect for deep fat frying. All of that phenolic stuff in the oil burns if the temperature gets too high. The cheaper olive oils are a reasonable compromise. The extra virgin oils contain the most phenols and may be healthier but the less than virgin olive oils work better for frying. They don't burn so easily. Plus plain olive oil is far cheaper than the extra virgin versions.


Cauliflower potato latke, a healthy compromise:

¼ head cauliflower steamed for awhile and cooled

2 Yukon gold potatoes

½ onion


3 eggs

¼ cup matzah meal



[i] Int J Oncol. 2004 Jan;24(1):187-92. Links

Targeting cell cycle machinery as a molecular mechanism of sulforaphane in prostate cancer prevention.

•  Wang L ,

•  Liu D ,

•  Ahmed T ,

•  Chung FL ,

•  Conaway C ,

•  Chiao JW .

Division of Medical Oncology, Mount Sinai Medical Center, New York , NY 10029 , USA .

Epidemiological studies recently concluded that consumption of cruciferous vegetables such as broccoli, cabbage, and cauliflower, etc. is inversely related to prostate cancer risk, although the mechanism of prevention and the responsible phytochemicals are unknown. Since clinically significant prostate cancer eventually can grow independent of androgen, the association of the growth and tumorigenesis of such prostate cancer cells with sulforaphane (SFN) which is a predominant isothiocyanate in cruciferous vegetables, investigated. These vegetables contain high concentrations of glucosinolate glucoraphanin, which yield sulforaphane when hydrolyzed by the plant enzyme myrosinase. This study showed that exposure of human androgen-independent DU-145 prostate cancer cells to SFN resulted in the inhibition of growth and tumorigenesis, as revealed by a reduction in cell density, DNA synthesis, and clonogenesis. Analyses of the mechanism revealed that SFN mediated cell cycle arrest by modulating the expression and functions of cell cycle regulators. SFN induced signals that inhibited the activity of cyclin-dependent kinase cdk4 with an up-stream induction of cdk inhibitor p21WAF-1/Cip-1, and reduced cyclin D1. The inhibition of cdk kinase activity could be affected with <1 micro M SFN within 24 h. As a result, phosphorylation of Rb proteins, which activates the transition from G1- to S-phase, was significantly decreased and the cell cycle progression retarded. SFN also down-regulated the expression of bcl-2, a suppressor of apoptosis, and activated caspases to execute apoptosis in the prostate cancer cells. The regulators of cell cycle have thus been revealed as targets of sulforaphane for growth arrest and apoptosis induction. The potential of SFN, as an active dietary factor to inhibit initiation and post-initiation of prostate cancer carcinogenesis is discussed.


[ii] Int J Oncol. 2006 Oct;29(4):883-8. Links

Effect of sulforaphane on cell growth, G(0)/G(1) phase cell progression and apoptosis in human bladder cancer T24 cells.

•  Shan Y ,

•  Sun C ,

•  Zhao X ,

•  Wu K ,

•  Cassidy A ,

•  Bao Y .

Department of Nutrition and Food Hygiene, Public Health College , Harbin Medical University , Harbin 150081, P.R. China.

Isothiocyanates (ITCs) from cruciferous vegetables have been shown to be effective in blocking initiation as well as progression of a range of chemically-induced tumors in animal models. In this study, sulforaphane, the most extensively studied ITC, was found to suppress the growth of T24 bladder cancer cells in vitro in a dose-dependent manner. Sulforaphane inhibited the proliferation of T24 cells with IC(5)0 values 26.9 and 15.9 microM following 24 and 48 h treatments. Sulforaphane (5-20 microM) induced early apoptosis and blocked cell cycle progression at G(0)/G(1) phase which was associated with upregulation of cyclin-dependent kinase inhibitor p27 expression. These results support a role for sulforaphane as an effective agent in the chemoprevention of bladder cancer.

PMID: 16964384 [PubMed - in process]


[iii] Mutat Res. 2006 Jul 25;599(1-2):76-87. Epub 2006 Feb 24. Click here to read  Links

Comparison of growth inhibition profiles and mechanisms of apoptosis induction in human colon cancer cell lines by isothiocyanates and indoles from Brassicaceae.

•  Pappa G ,

•  Lichtenberg M ,

•  Iori R ,

•  Barillari J ,

•  Bartsch H ,

•  Gerhauser C .

Division of Toxicology and Cancer Risk Factors, German Cancer Research Center , DKFZ, 69120 Heidelberg , Germany .

The isothiocyanates sulforaphane and PEITC (beta-phenethyl isothiocyanate) as well as the indoles indole-3-carbinol and its condensation product 3,3'-diindolylmethane are known to inhibit cancer cell proliferation and induce apoptosis. In this study, we compared the cell growth inhibitory potential of the four compounds on the p53 wild type human colon cancer cell line 40-16 (p53(+/+)) and its p53 knockout derivative 379.2 (p53(-/-)) (both derived from HCT116). Using sulforhodamin B staining to assess cell proliferation, we found that the isothiocyanates were strongly cytotoxic, whereas the indoles inhibited cell growth in a cytostatic manner. Half-maximal inhibitory concentrations of all four compounds in both cell lines ranged from 5-15 microM after 24, 48 and 72 h of treatment. Apoptosis induction was analyzed by immunoblotting of poly(ADP-ribose)polymerase (PARP). Treatment with sulforaphane (15 microM), PEITC (10 microM), indole-3-carbinol (10 microM) and 3,3'-diindolylmethane (10 microM) induced PARP cleavage after 24 and 48 h in both 40-16 and the 379.2 cell lines, suggestive of a p53-independent mechanism of apoptosis induction. In cultured 40-16 cells, activation of caspase-9 and -7 detected by Western blotting indicated involvement of the mitochondrial pathway. We detected time- and concentration-dependent changes in protein expression of anti-apoptotic Bcl-x(L) as well as pro-apoptotic Bax and Bak proteins. Of note is that for sulforaphane only, ratios of pro- to anti-apoptotic Bcl-2 family protein levels directly correlated with apoptosis induction measured by PARP cleavage. Taken together, we demonstrated that the glucosinolate breakdown products investigated in this study have distinct profiles of cell growth inhibition, potential to induce p53-independent apoptosis and to modulate Bcl-2 family protein expression in human colon cancer cell lines.

PMID: 16500682 [PubMed - indexed for MEDLINE]


[iv] Mutat Res. 2006 Oct 10;601(1-2):92-101. Epub 2006 Jul 14.   Links

Sulforaphane increases the efficacy of doxorubicin in mouse fibroblasts characterized by p53 mutations.

•  Fimognari C ,

•  Nusse M ,

•  Lenzi M ,

•  Sciuscio D ,

•  Cantelli-Forti G ,

•  Hrelia P .

Department of Pharmacology, University of Bologna , Bologna , Italy .

One novel strategy for increasing cancer chemotherapy efficacy and reversing chemoresistance involves co-administration of natural chemopreventive compounds alongside standard chemotherapeutic protocols. Sulforaphane is a particularly promising chemopreventive agent, which has been shown to exert proapoptotic effects on tumor cells containing p53 mutations. The p53(Ser220) mutation has been implicated in reduced efficacy and drug resistance in the context of osteosarcomas and breast tumors treated with doxorubicin-based protocols. We investigated the effects of a combination of doxorubicin and sulforaphane on cell viability and apoptosis induction in fibroblasts characterized by different p53 status (p53 wild-type, p53 knock-out, and p53(Ser220) mutation), and identified some of the molecular pathways triggered by the drug combination. Very high concentrations of doxorubicin were necessary to decrease the viability of p53(Ser220) and p53 knock-out (but not wild-type) cells. Treatment of p53(Ser220) and p53 knock-out cells with doxorubicin did not induce apoptosis, also at very high concentrations (10muM). Sulforaphane restored chemosensitivity and induced apoptosis in doxorubicin-resistant p53(Ser220) and p53 knock-out cells, irrespective of p53 status. The induction of apoptosis was caspase-3 dependent and caspase-8 independent. Bongkrekic acid, a mitochondrial membrane stabilizer, partially prevented the effects of doxorubicin plus sulforaphane on mitochondrial permeability but was unable to prevent the induction of apoptosis. N-acetyl-cysteine, a glutathione precursor, blocked the induction of apoptosis by doxorubicin plus sulforaphane. Considering the negligible safety profile of sulforaphane, our findings could prompt innovative clinical studies designed to investigate whether its coadministration can enhance the efficacy of doxorubicin-based regimens.

PMID: 16843502 [PubMed - in process]


[v] Ann Intern Med. 2006 Sep 5;145(5):333-41.   Links

Summary for patients in:

Ann Intern Med. 2006 Sep 5;145(5):I53.

The effect of polyphenols in olive oil on heart disease risk factors: a randomized trial.

•  Covas MI ,

•  Nyyssonen K ,

•  Poulsen HE ,

•  Kaikkonen J ,

•  Zunft HJ ,

•  Kiesewetter H ,

•  Gaddi A ,

•  de la Torre R ,

•  Mursu J ,

•  Baumler H ,

•  Nascetti S ,

•  Salonen JT ,

•  Fito M ,

•  Virtanen J ,

•  Marrugat J ,

•  EUROLIVE Study Group .

Municipal Institute for Medical Research, Barcelona , Spain . mcovas@imim.es

BACKGROUND: Virgin olive oils are richer in phenolic content than refined olive oil. Small, randomized, crossover, controlled trials on the antioxidant effect of phenolic compounds from real-life daily doses of olive oil in humans have yielded conflicting results. Little information is available on the effect of the phenolic compounds of olive oil on plasma lipid levels. No international study with a large sample size has been done. OBJECTIVE: To evaluate whether the phenolic content of olive oil further benefits plasma lipid levels and lipid oxidative damage compared with monounsaturated acid content. DESIGN: Randomized, crossover, controlled trial. SETTING: 6 research centers from 5 European countries. PARTICIPANTS: 200 healthy male volunteers. MEASUREMENTS: Glucose levels, plasma lipid levels, oxidative damage to lipid levels, and endogenous and exogenous antioxidants at baseline and before and after each intervention. INTERVENTION: In a crossover study, participants were randomly assigned to 3 sequences of daily administration of 25 mL of 3 olive oils. Olive oils had low (2.7 mg/kg of olive oil), medium (164 mg/kg), or high (366 mg/kg) phenolic content but were otherwise similar. Intervention periods were 3 weeks preceded by 2-week washout periods. RESULTS: A linear increase in high-density lipoprotein (HDL) cholesterol levels was observed for low-, medium-, and high-polyphenol olive oil: mean change, 0.025 mmol/L (95% CI, 0.003 to 0.05 mmol/L), 0.032 mmol/L (CI, 0.005 to 0.05 mmol/L), and 0.045 mmol/L (CI, 0.02 to 0.06 mmol/L), respectively. Total cholesterol-HDL cholesterol ratio decreased linearly with the phenolic content of the olive oil. Triglyceride levels decreased by an average of 0.05 mmol/L for all olive oils. Oxidative stress markers decreased linearly with increasing phenolic content. Mean changes for oxidized low-density lipoprotein levels were 1.21 U/L (CI, -0.8 to 3.6 U/L), -1.48 U/L (-3.6 to 0.6 U/L), and -3.21 U/L (-5.1 to -0.8 U/L) for the low-, medium-, and high-polyphenol olive oil, respectively. LIMITATIONS: The olive oil may have interacted with other dietary components, participants' dietary intake was self-reported, and the intervention periods were short. CONCLUSIONS: Olive oil is more than a monounsaturated fat. Its phenolic content can also provide benefits for plasma lipid levels and oxidative damage. International Standard Randomised Controlled Trial number: ISRCTN09220811.

PMID: 16954359 [PubMed - indexed for MEDLINE]


[vi] J Clin Endocrinol Metab. 2006 Jun;91(6):2062-7. Epub 2006 Mar 14.   Links

Effects of fat on gastric emptying of and the glycemic, insulin, and incretin responses to a carbohydrate meal in type 2 diabetes.

•  Gentilcore D ,

•  Chaikomin R ,

•  Jones KL ,

•  Russo A ,

•  Feinle-Bisset C ,

•  Wishart JM ,

•  Rayner CK ,

•  Horowitz M .

University of Adelaide, Department of Medicine, Royal Adelaide Hospital, North Terrace, Adelaide, South Australia 5000, Australia.

CONTEXT: Gastric emptying (GE) is a major determinant of postprandial glycemia. Because the presence of fat in the small intestine inhibits GE, ingestion of fat may attenuate the glycemic response to carbohydrate. OBJECTIVE: The objective of this study was to evaluate the effect of patterns of fat consumption on GE and glucose, insulin, glucagon-like peptide-1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP) concentrations after a carbohydrate meal in type 2 diabetes. DESIGN: This was a randomized, cross-over study in which GE of a radioisotopically labeled potato meal was measured on 3 d. SETTING: The study was performed at the Royal Adelaide Hospital . PATIENTS: Six males with type 2 diabetes were studied. INTERVENTION: Subjects ingested 1) 30 ml water 30 min before the mashed potato (water), 2) 30 ml olive oil 30 min before the mashed potato (oil), or 3) 30 ml water 30 min before the mashed potato meal that contained 30 ml olive oil (water and oil). MAIN OUTCOME MEASURES: GE, blood glucose, plasma insulin, GLP-1, and GIP concentrations were the main outcome measures. RESULTS: GE was much slower with oil compared with both water (P < 0.0001) and water and oil (P < 0.05) and was slower after water and oil compared with water (P < 0.01). The postprandial rise in blood glucose was markedly delayed (P = 0.03), and peak glucose occurred later (P = 0.04) with oil compared with the two other meals. The rises in insulin and GIP were attenuated (P < 0.0001), whereas the GLP-1 response was greater (P = 0.0001), after oil. CONCLUSIONS: Ingestion of fat before a carbohydrate meal markedly slows GE and attenuates the postprandial rises in glucose, insulin, and GIP, but stimulates GLP-1, in type 2 diabetes.

PMID: 16537685 [PubMed - indexed for MEDLINE]


[vii] J Nutr Biochem. 2006 Oct 16; [Epub ahead of print]   Links

Olive oil preparation determines the atherosclerotic protection in apolipoprotein E knockout mice.

•  Acin S ,

•  Navarro MA ,

•  Perona JS ,

•  Arbones-Mainar JM ,

•  Surra JC ,

•  Guzman MA ,

•  Carnicer R ,

•  Arnal C ,

•  Orman I ,

•  Segovia JC ,

•  Osada J ,

•  Ruiz-Gutierrez V .

Departamento de Bioquimica y Biologia Molecular y Celular, Facultad de Veterinaria, Universidad de Zaragoza, E-50013 Zaragoza, Madrid.

Oils enriched in monounsaturated fatty acids do not seem to behave similarly in protecting against the development of atherosclerosis in animal models, which has been attributed to the presence of soluble phenolic compounds. To test the relevance of other components of oils in the prevention of atherosclerosis, two olive oils from the same cultivar devoid of soluble phenolic compounds were prepared using different procedures (pressure or centrifugation), characterized and fed to apolipoprotein E-deficient mice as 10% (w/w) of their diet. The 2 olive oils had similar levels of monounsaturated fatty acids and squalene, but they differed in their content of linoleic, phytosterols, tocopherols, triterpenes and waxes, which were particularly enriched in the test olive oil obtained by centrifugation. In mice that received a diet enriched in the olive oil derived through centrifugation, the progression of atherosclerosis was delayed compared to the mice that received standard olive oil. That effect was associated with decreases in plasma triglycerides, total and non-high-density lipoprotein cholesterol and isoprostane 8-iso-prostaglandin F(2alpha). Our results clearly indicate that the preparation of olive oil is crucial in determining its antiatherosclerotic effect, which extends beyond the presence of phenolic compounds. The test olive oil exerted its antiatherosclerotic effects by modifying plasma lipids and oxidative stress, and it might be a good candidate to replace other fats in functional foods.


[viii] Ann Intern Med. 2006 Jul 4;145(1):1-11.   Links

Summary for patients in:

Ann Intern Med. 2006 Jul 4;145(1):I11.

Effects of a Mediterranean-style diet on cardiovascular risk factors: a randomized trial.

•  Estruch R ,

•  Martinez-Gonzalez MA ,

•  Corella D ,

•  Salas-Salvado J ,

•  Ruiz-Gutierrez V ,

•  Covas MI ,

•  Fiol M ,

•  Gomez-Gracia E ,

•  Lopez-Sabater MC ,

•  Vinyoles E ,

•  Aros F ,

•  Conde M ,

•  Lahoz C ,

•  Lapetra J ,

•  Saez G ,

•  Ros E ;

•  PREDIMED Study Investigators .

Institut d'Investigacions Biomediques August Pi Sunyer, Municipal Institut for Medical Research, University of Barcelona, and Catalan Institute of Health, Barcelona, Spain. restruch@clinic.ub.es

BACKGROUND: The Mediterranean diet has been shown to have beneficial effects on cardiovascular risk factors. OBJECTIVE: To compare the short-term effects of 2 Mediterranean diets versus those of a low-fat diet on intermediate markers of cardiovascular risk. DESIGN: Substudy of a multicenter, randomized, primary prevention trial of cardiovascular disease (Prevencion con Dieta Mediterranea [PREDIMED] Study). SETTING: Primary care centers affiliated with 10 teaching hospitals. PARTICIPANTS: 772 asymptomatic persons 55 to 80 years of age at high cardiovascular risk who were recruited from October 2003 to March 2004. Interventions: Participants were assigned to a low-fat diet (n = 257) or to 1 of 2 Mediterranean diets. Those allocated to Mediterranean diets received nutritional education and either free virgin olive oil, 1 liter per week (n = 257), or free nuts, 30 g/d (n = 258). The authors evaluated outcome changes at 3 months. MEASUREMENTS: Body weight, blood pressure, lipid profile, glucose levels, and inflammatory molecules. RESULTS: The completion rate was 99.6%. Compared with the low-fat diet, the 2 Mediterranean diets produced beneficial changes in most outcomes. Compared with the low-fat diet, the mean changes in the Mediterranean diet with olive oil group and the Mediterranean diet with nuts group were -0.39 mmol/L (95% CI, -0.70 to -0.07 mmol/L) and -0.30 mmol/L (CI, -0.58 to -0.01 mmol/L), respectively, for plasma glucose levels; -5.9 mm Hg (CI, -8.7 to -3.1 mm Hg) and -7.1 mm Hg (CI, -10.0 to -4.1 mm Hg), respectively, for systolic blood pressure; and -0.38 (CI, -0.55 to -0.22) and - 0.26 (CI, -0.42 to -0.10), respectively, for the cholesterol-high-density lipoprotein cholesterol ratio. The Mediterranean diet with olive oil reduced C-reactive protein levels by 0.54 mg/L (CI, 1.04 to 0.03 mg/L) compared with the low-fat diet. LIMITATIONS: This short-term study did not focus on clinical outcomes. Nutritional education about low-fat diet was less intense than education about Mediterranean diets. CONCLUSION: Compared with a low-fat diet, Mediterranean diets supplemented with olive oil or nuts have beneficial effects on cardiovascular risk factors.

PMID: 16818923 [PubMed - indexed for MEDLINE]


Ask the Doctor:
What's the difference between naturopathy and homeopathy?

[click here for the answer]

Submit your question here.

Enter your email to recieve the latest Health and Wellness newsletters from the clinic.