Dr Michael Eades discusses the remarks of Dr. JoAnn Manson, who is describing the analysis of data from the Women's Health Initiative study showing an association between statin drugs and the development of diabetes.
Watch this video!
http://www.youtube.com/watch?v=hbSnE5ald-s&desktop_uri=/watch%3Fv%3DhbSnE5ald-s&nomobile=1
Showing posts with label WHI. Show all posts
Showing posts with label WHI. Show all posts
Saturday, September 7, 2013
Friday, July 12, 2013
Statin = substantial increase in diabetes risk in postmenopausal women
Statin Use and Risk of Diabetes Mellitus in Postmenopausal Women in the Women's Health Initiative
Methods The WHI recruited 161 808 postmenopausal women aged 50 to 79 years at 40 clinical centers across the United States from 1993 to 1998 with ongoing follow-up. The current analysis includes data through 2005. Statin use was captured at enrollment and year 3. Incident DM status was determined annually from enrollment. Cox proportional hazards models were used to estimate the risk of DM by statin use, with adjustments for propensity score and other potential confounding factors. Subgroup analyses by race/ethnicity, obesity status, and age group were conducted to uncover effect modification.
Results This investigation included 153 840 women without DM and no missing data at baseline. At baseline, 7.04% reported taking statin medication. There were 10 242 incident cases of self-reported DM over 1 004 466 person-years of follow-up. Statin use at baseline was associated with an increased risk of DM (hazard ratio [HR], 1.71; 95% CI, 1.61-1.83). This association remained after adjusting for other potential confounders (multivariate-adjusted HR, 1.48; 95% CI, 1.38-1.59) and was observed for all types of statin medications. Subset analyses evaluating the association of self-reported DM with longitudinal measures of statin use in 125 575 women confirmed these findings.
Conclusions Statin medication use in postmenopausal women is associated with an increased risk for DM. This may be a medication class effect. Further study by statin type and dose may reveal varying risk levels for new-onset DM in this population.
was performed to reduce the confounding effects of other factors in the evaluation of the association between statin use and DM risk within an observational study setting. Participant-specific propensity scores were estimated from a logistic regression model to predict the probability of statin prescription. Covariates considered for inclusion into the logistic regression model included age, BMI, self-report of hypertension, self-report of CVD, family history of DM, smoking status, and physical activity. The final propensity score model retained all covariates noted herein with the exception of physical activity, which was an insignificant predictor of statin use. The association between statin use and DM risk was evaluated in Cox PH models after adjusting for the estimated propensity score.
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Read the complete article here.
ABSTRACT
Background This study investigates whether the incidence of new-onset diabetes mellitus (DM) is associated with statin use among postmenopausal women participating in the Women's Health Initiative (WHI).
Methods The WHI recruited 161 808 postmenopausal women aged 50 to 79 years at 40 clinical centers across the United States from 1993 to 1998 with ongoing follow-up. The current analysis includes data through 2005. Statin use was captured at enrollment and year 3. Incident DM status was determined annually from enrollment. Cox proportional hazards models were used to estimate the risk of DM by statin use, with adjustments for propensity score and other potential confounding factors. Subgroup analyses by race/ethnicity, obesity status, and age group were conducted to uncover effect modification.
Results This investigation included 153 840 women without DM and no missing data at baseline. At baseline, 7.04% reported taking statin medication. There were 10 242 incident cases of self-reported DM over 1 004 466 person-years of follow-up. Statin use at baseline was associated with an increased risk of DM (hazard ratio [HR], 1.71; 95% CI, 1.61-1.83). This association remained after adjusting for other potential confounders (multivariate-adjusted HR, 1.48; 95% CI, 1.38-1.59) and was observed for all types of statin medications. Subset analyses evaluating the association of self-reported DM with longitudinal measures of statin use in 125 575 women confirmed these findings.
Conclusions Statin medication use in postmenopausal women is associated with an increased risk for DM. This may be a medication class effect. Further study by statin type and dose may reveal varying risk levels for new-onset DM in this population.
Given the success of statins in both primary and secondary prevention of cardiovascular morbidity and mortality,1- 6 their use is progressively increasing, especially among older Americans.7 With such widespread use, even small risks are apparent alongside benefits. One emerging risk is an increased incidence of diabetes mellitus (DM). There is evidence that incident DM associated with statin use may be more common in the elderly, in women, and in Asians.8- 12 A recent analysis suggests that preexisting metabolic risk factors control incident DM rate with statin medication.13 It is unclear if this risk varies with individual statins or if this is a dose-driven class effect.9,14 Although experimental and clinical studies find that individual statins act differently on glucose homeostasis as a function of relative lipophilicity and/or potency of action,15 other findings differ. A recent meta-analysis of 17 randomized controlled trials by Mills et al16 found a class effect increase of new-onset DM with statins (odds ratio [OR], 1.09; 95% CI, 1.02-1.16) similar to that reported by Sattar et al.9 Possibly, the grouping of statins masks the effect variation of individual statins. Still, at some given dose threshold, differences may be overcome, as implied by a meta-analysis of 5 trials comparing intensive to moderate dosing regimens using mainly atorvastatin and simvastatin.13,17 Notably, meta-analysis results display intertrial and intratrial variability in diagnostic and statistical methods and do not consistently consider confounding factors. Moreover, contributing sample sizes do not permit balanced comparison by statin type, sex, race/ethnicity, and age. Similarly, single studies may uncover only part of a greater topography.
As a large part of the aging population, postmenopausal women have not been fully represented in past clinical trials.16 Sex differences in DM pathogenesis are well recognized.18- 19 Using the Women's Health Initiative (WHI) data, we evaluated the overall effect of statin medication use on incident DM risk and examined these associations by specific statin agent. We stratified analyses by race/ethnicity, body mass index (BMI) (calculated as weight in kilograms divided by height in meters squared) category, and age group to determine if any associations were modified by these factors. In addition, we conducted subgroup analysis in women with and without self-reported cardiovascular disease (CVD) at baseline to address potential confounding and selection bias.
The WHI recruited 161 808 postmenopausal women aged 50 to 79 years at 40 clinical centers across the United States from 1993 to 1998 and followed consenting participants. Of these women, 68 132 were enrolled in 1, 2, or all 3 of the clinical trial (CT) arms: the Dietary Modification Trial, the Hormone Trial, and the Calcium and Vitamin D Trial. Another 93 676 women were enrolled into a prospective observational study (OS).20- 23 The WHI eligibility criteria included the ability to complete study visits with expected survival and local residency for at least 3 years. Original exclusion criteria addressed conditions that would limit full participation in the study. This analysis used WHI data through 2005. After exclusion for prevalent DM, missing data, and use of cerivastatin (this medication was withdrawn from the market in 2001 for safety reasons), a total of 153 840 women were included (Figure).
Figure. Flowchart for statin users and diabetes mellitus (DM) analyses using data sets from the Women's Health Initiative.
MEASUREMENT AND CLASSIFICATION OF STATIN MEDICATIONS
The current medication regimens of all CT participants were inventoried at baseline and at years 1, 3, 6, and 9. In the OS, medication data were inventoried at baseline and year 3. At each inventory, the brand or generic name on the medication label was matched to the corresponding item in the Master Drug Data Base (Medi-Span, Indianapolis, Indiana). We sorted for statin use as users or nonusers at baseline and year 3. Given that Sattar et al9 found a null effect of lipophilicity among statins, and in the absence of dose information, we determined statin categories by relative potency of action to decrease low-density lipoprotein cholesterol. Accordingly, statins were designated as low (fluvastatin, lovastatin, pravastatin) or high (simvastatin, atorvastatin) potency.24- 25
IDENTIFICATION OF DM
At baseline and at each semiannual (CT) or annual (OS) contact, incident treated DM was identified by questionnaire and was defined as a self-report of a new physician diagnosis of treated DM. This method of identification of prevalent and incident DM has been used in prior publications by the WHI investigators.18,26- 28 The accuracy of self-reported DM in the WHI trials has been assessed using medication and laboratory data, and self-reported DM was found to be reliable.29
COVARIATES
Baseline questionnaires ascertained demographic and health history information, including race/ethnicity, age, educational attainment, family history of DM, family history of depression, self-report of CVD, hormone therapy use, and smoking status. Baseline self-report for CVD has been previously validated in the WHI30- 31 and found to have reasonable agreement with hospital discharge International Classification of Diseases, Ninth Revision (ICD-9) codes.
The metabolic equivalents of physical activities and average daily nutrient intake were computed, using detailed methods described elsewhere.32- 33 Trained and certified clinic staff measured height using a fixed stadiometer and weight by a calibrated balance-beam scale. Relative weight as BMI was calculated from these values. Blood was analyzed for glucose and insulin for the random 6% WHI-CT blood subsample at baseline, year 1, year 3, year 6, and year 9. Fasting glucose was analyzed using the hexokinase method with interassay coefficients of variation less than 2%.26 Insulin was measured by enzyme-linked immunosorbent assay. The WHI used the homeostasis model assessment of insulin resistance (HOMA-IR), which was developed for application in large epidemiologic investigations as an alternative to the glucose clamp. HOMA-IR = fasting plasma insulin (μIU/mL) × fasting plasma glucose (mmol/L)/22.5.34
STATISTICAL ANALYSIS
Cox proportional hazards (PH) models were used to estimate hazard ratios (HRs) of DM by statin medication use. The dependent variable was time to occurrence of DM determined by self-report (ie, time to event). The time to event was calculated as the interval between enrollment date and the earliest of the following: (1) date of annual medical history update when new DM was ascertained (observed outcome) and (2) date of the last annual medical update during which DM status was ascertained (censored outcome). The primary independent variable in these analyses was statin use at baseline, coded as a binary variable. We present 3 Cox PH models to examine the association between baseline statin use and DM: model 1 estimates the unadjusted HRs (and associated 95% CIs) of the effects of statin use on incident DM; model 2 presents age- and race/ethnicity–adjusted HRs; and model 3 presents HRs adjusted for all potential confounding variables at baseline (age, race/ethnicity, education, cigarette smoking, BMI, physical activity, alcohol intake, energy intake, family history of DM, hormone therapy use, study arm, and self-report of CVD). Similar analyses were conducted for specific type of statin medication use at baseline, categorized as low vs high potency.
Since individuals using statins may have different underlying conditions that could put them at elevated risk for DM, we conducted several subgroup analyses to control confounding by indication. First, we conducted subgroup analyses by age, race/ethnicity, and BMI categories to examine whether the associations of statin use and onset of DM differed by categories of these variables. Age was categorized into 3 groups (50-59 years, 60-69 years, and ≥70 years). Race/ethnicity was assessed according to 4 major groups (white, African American, Hispanic, Asian). Body mass index was categorized into 3 groups (<25 .0="" 25.0-29.9="" 2="" analyses="" analysis="" at="" baseline.="" conducted="" cvd="" either="" finally="" in="" of="" or="" propensity="" score="" second="" self-reported="" similar="" subgroups="" sup="" we="" with="" without="" women="">35
After exclusion for cases of DM before year 3 (146 women), use of cerivastatin (651 women), and missing medication data at year 3 (2 women), our longitudinal analyses were conducted in a subset of 125 575 women from the OS and the CT arm at baseline and year 3 visits. Statin use was sorted into 4 categories: (1) never took statin; (2) use at both baseline and at the year 3 visit, (3) use only at baseline; and (4) use only at the year 3 visit. The HRs for DM by statin use were estimated similarly based on Cox PH models.
Participant characteristics are listed in Table 1. At baseline, the mean (SD) age of women included in our sample was 63.2 (7.3) years. Approximately 16.30% of the women were from racial/ethnic groups other than white, of which the largest representation was African American (8.32%). Only 2.56% (3922 women) were Asian. At baseline, 7.04% of participants took statin medication. Of these, 30.29% took simvastatin; 27.29%, lovastatin; 22.52%, pravastatin; 12.15%, fluvastatin; and 7.74%, atorvastatin. Comparison between statin users and nonusers showed significant differences in baseline characteristics.
A total of 10 242 incident cases of DM were reported over 1 004 466 person-years of follow-up. Table 2 presents results regarding the association between statin use at baseline and risk of incident DM. In unadjusted models, statin use at baseline was significantly associated with an increased DM risk (HR, 1.71; 95% CI, 1.61-1.83) when compared with nonuse. This association was decreased but remained significant after adjusting for potential confounders (HR, 1.48; 95% CI, 1.38-1.59). This association was observed for all types of statin. Similar risk associations were found in use of either high- or low-potency statins, with multivariate-adjusted HRs of 1.45 (95% CI, 1.36-1.61) and 1.48 (95% CI, 1.36-1.61) compared with nonusers, respectively. Table 3 shows subgroup analyses by race/ethnicity, BMI category, and age group. In both unadjusted and adjusted models, statin use was consistently associated with increased risk of DM across subgroups by age. We observed significantly increased risk of DM by statin use within subgroups of white, Hispanic, and Asian women in both unadjusted and adjusted models. In adjusted models, we observed HRs of 1.49 (95% CI, 1.38-1.62), 1.18 (95% CI, 0.96-1.45), 1.57 (95% CI, 1.14-2.17), and 1.78 (95% CI, 1.32-2.40) among whites, African Americans, Hispanics, and Asians, respectively. Statin use was also associated with a significantly increased risk of DM within 3 subgroups according to BMI (<25 .0="" 1.09-1.33="" 1.20="" 1.48-1.87="" 1.57-2.29="" 1.66="" 1.89="" 25.0-29.9="" 25.0="" 29.9="" 30.0="" a="" adjusted="" adjusting="" after="" all="" among="" and="" associated="" bmi="" ci="" compared="" confounders.="" dm="" for="" groups="" higher="" hrs="" in="" increased="" less="" lower="" models="" moreover="" observed="" of="" or="" p="" potential="" respectively.="" risk="" significantly="" statin="" than="" the="" to="" use="" was="" were="" when="" with="" within="" women="">
To address potential confounding and selection bias, we conducted subgroup analyses among postmenopausal women with and without a history of CVD (Table 4). Among a subset of 24 842 women who self-reported CVD at baseline, we found that statin use was associated with an increased risk of DM (HR, 1.52; 95% CI, 1.36-1.71). These associations remained significant after adjusting for potential confounders (HR, 1.46; 95% CI, 1.29-1.65). Similar findings were observed among women without CVD at baseline.
In unadjusted models, statin use was significantly related to DM risk (HR, 1.71; 95% CI, 1.61-1.83). When the propensity score was included, the estimated HR attenuated to 1.38 (95% CI, 1.29-1.47). On inclusion of other confounders in the model, the HR was essentially unaltered (HR, 1.40; 95% CI, 1.31-1.51). Propensity score adjusted models yielded HRs of 1.38 (95% CI, 1.23-1.54) and 1.40 (95% CI, 1.29-1.53) for respective increased risk with either high- or low-potency statin use at baseline compared with nonuse.
LONGITUDINAL MEASURES OF STATIN USE AND RISK OF DM
When compared with those who never received statin therapy, unadjusted HRs of 1.82 (95% CI, 1.65-2.00), 1.75 (95% CI, 1.43-2.14), and 1.81 (95% CI, 1.67-1.97) were observed for the groups of women who reported statin use at both baseline and at the year 3 visit, reported statin use only at baseline, and reported statin use only at the year 3 visit, respectively (Table 5). The risk associations remained significant after adjusting for age, race/ethnicity, other potential confounders, and propensity score. The multivariate adjusted HRs were 1.47 (95% CI, 1.32-1.64), 1.44 (95% CI, 1.15-1.80), and 1.60 (95% CI, 1.47-1.75), respectively.
SENSITIVITY ANALYSIS
A sensitivity analysis was conducted on a subset of 3706 women without DM at baseline and enrolled in the WHI CT for whom fasting glucose measurements were available at baseline and at least 1 additional follow-up visit. Diabetes mellitus was identified based on fasting glucose levels of 126 mg/dL (6.99 mmol/L) or higher. In unadjusted models, statin use at baseline was not significantly related to DM risk (HR, 1.06; 95% CI, 0.61-1.86). However, using baseline through year 6 data in the CT arm, we found that the statin users had higher fasting glucose levels and HOMA-IR compared with non–statin users, with increasing values from baseline to year 6 follow-up.
Read the complete article here.
Tuesday, February 21, 2012
Statin Drugs Raise the Risk for Diabetes in Postmenopausal Women by 48%
Statin Drugs Raise the Risk for Diabetes in Postmenopausal Women by 48%
Older women using Statin Drugs like Lipitor may be at a 48% higher risk for becoming Type 2 Diabetics. This result was published in the Archives of Internal Medicine and reported by Medpage Today, January 9, 2012. The study didn’t specifically prove that statins cause Diabetes but rather proved that either the use of statins causes Diabetes or that statin use is somehow related to the incidence of Diabetes. Future studies will be needed to prove any cause/effect relationships.This is yet another “shot across the bow” at the statin drug industry which has convinced many Americans that they have to take statins for their cardiovascular health. I stopped taking Lipitor months ago because I deemed the risk much greater than the benefit – and my physician went along with it because of my weight loss with a low carb diet. To acquaint you with the dark side of statins and why many are doing as I have, watch the following video by Dr. Diamond. He covers statins starting at 33:45 into the clip. His presentation is backed up by data and references from the University of South Florida.
In terms of the 48% higher risk figure, it is important to realize that this is called a Hazard Risk and is a ratio of a ratio, masking some important issues. You need to consider a simpler perspective of the data to meaningfully assess what this means. I don’t have the exact figures, but based on the published study data, the likelihood of all the women in the study becoming Diabetic was around 6.7%. The women on statins were (based on the study results) found to have a 48% higher risk of becoming diabetic. The rough estimate of the likelihood of women on statins to become diabetic was therefore 148% of 6.7%, or 9.9%. From this simpler perspective the numbers aren’t so frightening. In other words, for these women, going on a statin increased the likelihood of Diabetes by 3.2%, from 6.7% to 9.9%. It is still, however, a finding that is not good news for patients on statins.
Getting back to the new statin study: Yunsheng Ma, MD, PhD, of the University of Massachusetts School of Medicine, was intrigued by prior research that suggested a link between statins and Diabetes and established an estimate of a 9% higher risk of Diabetes for statin users. Based on this, Dr. Ma and his colleagues decided to investigate further with an analysis of the data from a large study called the Women’s Health Initiative. After that analysis, in short, they found a much higher risk for Diabetes, for postmenopausal women on statins.
The Women’s Health Initiative provided data on 153,840 women with an average age of 63, who didn’t have Diabetes when they entered the study in 1993. About 7% of the women were on statins at the beginning of the study. Analysis of the women on statins compared to women not on statins yielded a 48% greater risk of the onset of Type 2 Diabetes during the study, which was last analyzed in 2005. This result was obtained after analysis adjustments were made to make sure that issues like age, race, and weight weren’t contributing factors. The 48% higher risk was seen for all types of statins (for example Lipitor, Crestor, Zocor, and Mevacor).
Since the study didn’t conclusively find that statins cause Diabetes, the researchers were clear in recommending that patients consult with their doctors on this issue before changing their medications. They did suggest, however, that since there is a higher risk of Diabetes with statin users, patients should strongly consider lifestyle change (such as weight loss and exercise) to improve their health rather than think that they can, “without risk”, just take the easy approach with statins.
Some interesting things are going on with the TV News coverage. Yesterday NBC reported on the study mentioned here, using the 48% increased risk factor (Hazard Risk). On the Today Show today, however, NBC reported on the same story but chose to report the numbers from the “simpler perspective” with no mention of the Hazard Factor 48% number. They reported that the likelihood of women becoming Diabetic was 10% for women who were on statins but only 6.4% for women who weren’t. That doesn’t look so frightening does it? I wonder if the change from the Hazard Risk to the less frightening simple perspective had anything to do with the minute-long Lipitor commercial that NBC aired during the show!
It’s ironic that the supporters of statin drugs may have pulled the same trick (but in reverse) when they put together the original clinical study analysis that got us onto statins in the first place. See the video above from Dr. Diamond at around 37:30 into the clip. The detailed analysis results indicated that reducing cholesterol lowered the likelihood of death by Coronary Heart Disease from 2% to 1.6% (only 0.4%) – not very exciting. The statin supporters however proclaimed that it was a 24% reduction in risk (Hazard Risk)!
This post is featured on the Modern Paleo Blog.
From: http://cravingsugar.net/statin-drug-study-reveals-48-increased-risk-diabetes-women-lipitor.php
Thursday, February 10, 2011
Saturated Fat and Heart Disease
Dwight C. Lundell M.D. has an article at SpaceDoc that reaffirms an important yet under reported fact:
'There never has been any direct evidence that saturated fat caused heart disease or even a mechanism whereby heart disease would happen.'
===================================================
Saturated Fat and Heart Disease
by Dwight C. Lundell M.D.
Does the thought of a steak, bacon and eggs, or real milk make you cringe thinking you're instantly clogging up your arteries? How many times have you seen physicians and nutritionists write "artery clogging saturated fats"? For the last 40 years the dietary instructions from governments and other authoritative bodies have told us to avoid all animal fats.
Americans took the message seriously and complied. Average fat consumption decreased, average blood cholesterol levels decreased but their rate of heart disease has continued to rise; the cost of its treatment has continued to rise. Now, in 2011 we have 24 MILLION people diagnosed with diabetes and another 65 million with pre-diabetes and an epidemic of obesity now afflicting over 65% of the population.
The evidence continues to mount that there's no benefit and probable harm from a low fat diet. Two recent examples, the Women's Health Initiative which studied 48,835 women demonstrating no benefit from a low fat diet in terms of heart disease or breast cancer. (Ref 1 ).
The Nurses' Health Study which has followed 90,000 female health professionals, once again demonstrated no reduction in heart disease or cancer, from a low-fat diet. ( Ref 2 ).
Even the famous Framingham study now admits there is no association between dietary fat and heart disease and indeed the association of elevated cholesterol and heart disease is limited to a small segment of the study population. ( Ref 3 ).
The January 2009 American Heart Journal reported that of the 137,000 people admitted to over 500 hospitals in the United States with heart attack, nearly 75% had "normal" LDL cholesterol levels, that is below 130 ( see cholesterol converter for mg / dL to mmol / L conversion ).
The evidence against saturated fat has always been circumstantial. That is, saturated fat was said to elevate blood cholesterol and elevated blood cholesterol was said to cause heart disease therefore saturated fat would cause heart disease. There never has been any direct evidence that saturated fat caused heart disease or even a mechanism whereby heart disease would happen.
Although there are more than a dozen types of saturated fat, humans predominantly consume three; stearic acid, palmitic acid, and lauric acid. These three fats make up 95% of the saturated fat in a piece of prime rib, a slice of bacon, a piece of chicken skin, and nearly 70% of that in butter and whole milk.
It is well established that stearic acid has no affect on cholesterol levels. In fact stearic acid is converted in the liver to oleic acid which is monounsaturated like olive oil and said to be healthy. Most scientists now consider stearic acid to be benign or potentially beneficial. Palmitic and lauric acid do raise LDL cholesterol levels, but they also raise HDL cholesterol levels, and therefore may be beneficial.
Still worried about clogging up your arteries? The question reflects how most people today have become conditioned to eliminate fat from their diet for fear of clogging their arteries. With doctors and medical establishments recommending the elimination of saturated fat, nutritionists and other authors repeating the phrase "artery clogging saturated fats" the media certainly follows and we have formed a deep ingrained belief that saturated fat is evil and unhealthy.
In March of 2009, researchers from the U.S. National Cancer Institute reported that those whose diets contained the highest proportion of red or processed meat had a higher overall risk of death and specifically a higher risk of cancer and heart disease than those who ate the least processed or red meat. ( Ref 4 ).
The press had a field day as the news circulated the wires quickly. Here are a few of the headlines:
"Eating red meat linked to early death, study finds"
"Study shows red meat consumption linked to higher risk of dying from cancer, heart disease"
"Death linked to too much red meat"
Dr. Michael R. Eades wrote a brilliant reply to the fault in this study and the media overreaction in a blog titled Meat and Mortality. ( Ref 5 ).
Here is a brief excerpt:
"At the same time that this paper appeared, showing increased red meat consumption to be tied to a slight increased risk of death (and showing that those subjects eating white meat had less risk), a couple of other papers came out in the online pre-publication section of the American Journal of Clinical Nutrition (AJCN), arguably the world's most prestigious nutritional scientific journal.
These two AJCN papers saw the light of day at around the same time as this highly-publicized study on meat and mortality, but demonstrated the opposite results. They got no press coverage whatsoever. Which proves what I've been saying all along: the press is biased against meat in general, and especially against red meat."
I completely agree with Dr. Eades about the media bias and am surprised by authors who should know better and continue to write "artery clogging saturated fats".
The most recent definitive study of all the competent studies regarding saturated fats and heart disease called a meta-analysis and published in the AJCN January 13, 2010 shows that over a 5 to 23 year follow-up of 347,747 subjects, there is no association between the intake of saturated fat and heart disease or stroke.( Ref 6 ).
The bottom line is that there is no connection between the intake of saturated fat and heart disease or stroke. But there is a connection between the currently recommended high carbohydrate diet and heart disease and stroke.
So enjoy bacon and eggs and forgo the oatmeal and bagels, your LDL will come down your HDL will go up, your weight will go down and your satisfaction with your diet will go up. The low fat diet is the worst dietary advice in the last 50 years and it is the proximate cause of our epidemics of heart disease, diabetes and obesity.
Accurate knowledge cannot come from reading abstracts of articles or reporters' interpretation of the abstract.
Dwight C. Lundell M.D.
http://www.thecureforheartdisease.net/
Chief Medical Consultant, Asantae Inc.
Chief Medical Consultant at www.realweight.com
Dr. Lundell's experience in Cardiovascular & Thoracic Surgery over the last 25 years includes certification by the American Board of Surgery, the American Board of Thoracic Surgery, and the Society of Thoracic Surgeons.
Dr. Lundell was a pioneer in off-pump coronary artery bypass or "beating heart" surgery reducing surgical complications and recovery times.
He has served as Chief resident at the University of Arizona and Yale University Hospitals and later served as Chief of Staff and Chief of Surgery.
He was one of the founding partners of the Lutheran Heart Hospital which became the second largest Heart hospital in the U.S.
Ref 1. http://www.pcrm.org/health/prevmed/pdfs/modest_diet.pdf
Ref 2. http://www.channing.harvard.edu/nhs/
Ref 3. http://www.framinghamheartstudy.org/
Ref 4. http://www.ncbi.nlm.nih.gov/pubmed/19307518
Ref 5. http://www.proteinpower.com/drmike/fast-food/meat-and-mortality/
Ref 6. http://www.ajcn.org/content/early/2010/01/13/ajcn.2009.27725.abstract
'There never has been any direct evidence that saturated fat caused heart disease or even a mechanism whereby heart disease would happen.'
===================================================
Saturated Fat and Heart Disease
by Dwight C. Lundell M.D.
Does the thought of a steak, bacon and eggs, or real milk make you cringe thinking you're instantly clogging up your arteries? How many times have you seen physicians and nutritionists write "artery clogging saturated fats"? For the last 40 years the dietary instructions from governments and other authoritative bodies have told us to avoid all animal fats.
Americans took the message seriously and complied. Average fat consumption decreased, average blood cholesterol levels decreased but their rate of heart disease has continued to rise; the cost of its treatment has continued to rise. Now, in 2011 we have 24 MILLION people diagnosed with diabetes and another 65 million with pre-diabetes and an epidemic of obesity now afflicting over 65% of the population.
The evidence continues to mount that there's no benefit and probable harm from a low fat diet. Two recent examples, the Women's Health Initiative which studied 48,835 women demonstrating no benefit from a low fat diet in terms of heart disease or breast cancer. (Ref 1 ).
The Nurses' Health Study which has followed 90,000 female health professionals, once again demonstrated no reduction in heart disease or cancer, from a low-fat diet. ( Ref 2 ).
Even the famous Framingham study now admits there is no association between dietary fat and heart disease and indeed the association of elevated cholesterol and heart disease is limited to a small segment of the study population. ( Ref 3 ).
The January 2009 American Heart Journal reported that of the 137,000 people admitted to over 500 hospitals in the United States with heart attack, nearly 75% had "normal" LDL cholesterol levels, that is below 130 ( see cholesterol converter for mg / dL to mmol / L conversion ).
The evidence against saturated fat has always been circumstantial. That is, saturated fat was said to elevate blood cholesterol and elevated blood cholesterol was said to cause heart disease therefore saturated fat would cause heart disease. There never has been any direct evidence that saturated fat caused heart disease or even a mechanism whereby heart disease would happen.
Although there are more than a dozen types of saturated fat, humans predominantly consume three; stearic acid, palmitic acid, and lauric acid. These three fats make up 95% of the saturated fat in a piece of prime rib, a slice of bacon, a piece of chicken skin, and nearly 70% of that in butter and whole milk.
It is well established that stearic acid has no affect on cholesterol levels. In fact stearic acid is converted in the liver to oleic acid which is monounsaturated like olive oil and said to be healthy. Most scientists now consider stearic acid to be benign or potentially beneficial. Palmitic and lauric acid do raise LDL cholesterol levels, but they also raise HDL cholesterol levels, and therefore may be beneficial.
Still worried about clogging up your arteries? The question reflects how most people today have become conditioned to eliminate fat from their diet for fear of clogging their arteries. With doctors and medical establishments recommending the elimination of saturated fat, nutritionists and other authors repeating the phrase "artery clogging saturated fats" the media certainly follows and we have formed a deep ingrained belief that saturated fat is evil and unhealthy.
In March of 2009, researchers from the U.S. National Cancer Institute reported that those whose diets contained the highest proportion of red or processed meat had a higher overall risk of death and specifically a higher risk of cancer and heart disease than those who ate the least processed or red meat. ( Ref 4 ).
The press had a field day as the news circulated the wires quickly. Here are a few of the headlines:
"Eating red meat linked to early death, study finds"
"Study shows red meat consumption linked to higher risk of dying from cancer, heart disease"
"Death linked to too much red meat"
Dr. Michael R. Eades wrote a brilliant reply to the fault in this study and the media overreaction in a blog titled Meat and Mortality. ( Ref 5 ).
Here is a brief excerpt:
"At the same time that this paper appeared, showing increased red meat consumption to be tied to a slight increased risk of death (and showing that those subjects eating white meat had less risk), a couple of other papers came out in the online pre-publication section of the American Journal of Clinical Nutrition (AJCN), arguably the world's most prestigious nutritional scientific journal.
These two AJCN papers saw the light of day at around the same time as this highly-publicized study on meat and mortality, but demonstrated the opposite results. They got no press coverage whatsoever. Which proves what I've been saying all along: the press is biased against meat in general, and especially against red meat."
I completely agree with Dr. Eades about the media bias and am surprised by authors who should know better and continue to write "artery clogging saturated fats".
The most recent definitive study of all the competent studies regarding saturated fats and heart disease called a meta-analysis and published in the AJCN January 13, 2010 shows that over a 5 to 23 year follow-up of 347,747 subjects, there is no association between the intake of saturated fat and heart disease or stroke.( Ref 6 ).
The bottom line is that there is no connection between the intake of saturated fat and heart disease or stroke. But there is a connection between the currently recommended high carbohydrate diet and heart disease and stroke.
So enjoy bacon and eggs and forgo the oatmeal and bagels, your LDL will come down your HDL will go up, your weight will go down and your satisfaction with your diet will go up. The low fat diet is the worst dietary advice in the last 50 years and it is the proximate cause of our epidemics of heart disease, diabetes and obesity.
Accurate knowledge cannot come from reading abstracts of articles or reporters' interpretation of the abstract.
Dwight C. Lundell M.D.
http://www.thecureforheartdisease.net/
Chief Medical Consultant, Asantae Inc.
Chief Medical Consultant at www.realweight.com
Dr. Lundell's experience in Cardiovascular & Thoracic Surgery over the last 25 years includes certification by the American Board of Surgery, the American Board of Thoracic Surgery, and the Society of Thoracic Surgeons.
Dr. Lundell was a pioneer in off-pump coronary artery bypass or "beating heart" surgery reducing surgical complications and recovery times.
He has served as Chief resident at the University of Arizona and Yale University Hospitals and later served as Chief of Staff and Chief of Surgery.
He was one of the founding partners of the Lutheran Heart Hospital which became the second largest Heart hospital in the U.S.
Ref 1. http://www.pcrm.org/health/prevmed/pdfs/modest_diet.pdf
Ref 2. http://www.channing.harvard.edu/nhs/
Ref 3. http://www.framinghamheartstudy.org/
Ref 4. http://www.ncbi.nlm.nih.gov/pubmed/19307518
Ref 5. http://www.proteinpower.com/drmike/fast-food/meat-and-mortality/
Ref 6. http://www.ajcn.org/content/early/2010/01/13/ajcn.2009.27725.abstract
Monday, November 26, 2007
A lesson from "Women’s Health Initiative (WHI) Dietary Modification Trial. "
Sandy Szwarc states the purpose of her blog Junkfood Science to be:
"Critical examinations of studies and news on food, weight, health and healthcare that mainstream media misses. Debunks popular myths, explains science and exposes fraud that affects your health. Plus some fun food for thought. For readers not afraid to question and think critically to get to the truth."
She then discusses some results of the WHI that didn't seem to make headlines. It's a good read and quite informative. Read her full article HERE.
"Critical examinations of studies and news on food, weight, health and healthcare that mainstream media misses. Debunks popular myths, explains science and exposes fraud that affects your health. Plus some fun food for thought. For readers not afraid to question and think critically to get to the truth."
She then discusses some results of the WHI that didn't seem to make headlines. It's a good read and quite informative. Read her full article HERE.
Sunday, March 25, 2007
Why the Low-Fat Diet is Stupid and Potentially Dangerous
Be it known there is controversy in this subject. Here is a scholarly, well written and well documented article that bears scrutiny. Verify what he says and if, as he states, the evidence is significant, act on it. Note that the last 1/3 of this article is composed of references so please do your Due-Diligence. Though it's a bit long I believe it is worth the read. Else I would not have posted it in its entirety.
Here is a quote from near the end of the article. "NOTE: I have no problem with people reprinting this article on other web sites for non-commercial purposes. Heck, you can post it on the side of the Empire State Building for all I care (just be sure to seek permission from the owners first). However, PLEASE ENSURE that you give full credit to the author, whether you reproduce the article in whole or part."
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Why the Low-Fat Diet is Stupid and Potentially Dangerous
Anthony Colpo, February 23, 2006.
On February 8, 2006, the Journal of the American Medical Association delivered a huge blow to advocates of low-fat 'nutrition' by publishing the results of the huge Women's Health Initiative trial. The results of the trial clearly showed that a low-fat diet failed to prevent cardiovascular disease or cancer in women even when followed continuously for eight years. In women with pre-existing CVD, the low-fat diet increased the risk of CVD by 26 percent!Since the publication of the WHI results, low-fat diet supporters have been working overtime manufacturing excuses for the failure of their beloved regimen. Foremost among these is that the women in the low-fat group did not reduce their fat intake sufficiently. I even had one sadly misguided soul write to me the other day telling me I did not "understand" low-fat diets, that the only reason they frequently fail is because people following them don't lower their fat intake enough.
Such stupidity makes my head spin…
First of all, I understand low-fat diets only too well! Much to my regret, I followed one throughout most of the nineties, and the result was nothing short of disastrous.
My low-fat nightmare began in my early twenties, after a doctor told me that my cholesterol, at 213, was "moderately high" and placed me at increased risk of heart disease (something I now know to be nonsense). Following the prevailing dietary wisdom at the time, I soon adopted a low-fat diet. This wasn't your average low-fat diet--it was a VERY low-fat diet, with the kind of anemic fat intake that wouild have made lipid-phobes like Ornish and Pritikin proud.
For years, I ate only the leanest meats; in fact, to this day, the thought of eating another skinless chicken breast, kangaroo steak, or low-fat fish makes me want to puke! Fuelling the high energy demands of my daily workouts in the face of a low fat intake meant eating carbohydrates--lots of them! In keeping with the common advice still given to athletes to eat lots of 'healthy' complex carbohydrate foods, I consumed copious amounts of rye bread, brown rice, sweet potato, wholemeal pasta, rolled oats, buckwheat, and millet.
My dedication to the low-fat mantra was nothing short of religious, and my low-fat brainwashing so thorough that when I sat down and calculated the average amount of fat calories I was taking in, I was actually proud when I realized I was consistently consuming less than ten percent of my calories as fat every day!
Halfway through the nineties, reality began to bite--hard. Despite my 'healthy' diet, and my daily strenuous training regimen, my blood pressure had risen from 110/65, a reading characteristic of highly-conditioned athletes, to an elevated 130/90. I noticed it was becoming increasingly harder to maintain the lean, "ripped", vascular look that I had always prided myself on. Instead, my physique was becoming increasingly smooth and bloated. My digestive system became progressively more sluggish, my stomach often feeling heavy and distended after meals. I frequently felt tired after meals. I showed signs of leaky gut syndrome, racking up a rather impressive list of irreversible food sensitivities. I had never been much of a coffee drinker, but I was now frequently trying to fight off increasing fatigue by sipping a strong black or two before training sessions. My fasting blood glucose level was below the normal range, indicative of reactive hypoglycemia.
Basically, I felt like crap!
It wasn't until I abandoned the whole low-fat charade, and adopted a diet that went against everything preached by the reigning diet orthodoxy, that I began to reverse these symptoms. When I ate more saturated fat and meat than ever before and subsequently felt better than ever before, I quickly realized that most diet 'experts' actually had no clue what they were talking about. I quickly realized that they were mere parrots repeating an official party line.
When I look back on my fat-fearing days, where I really believed that dietary fat was some sort of heinous toxin, the first thought that comes to mind is "What a wanker!" I then think of the sad legion of brainwashed folks all around the world who still follow the idiotic low-fat paradigm. "Poor folks," I think to myself, "they really have no idea just how badly they've been had…"
While I feel sorry for many of these folks, I have nothing but utter contempt for those who write me in defense of the low-fat paradigm. To be fooled is one thing, but to vigorously defend those who have mercilessly deceived and shafted you is beyond pitiful--such self-destructive stupidity is an absolutely repugnant thing to observe!
Let's now find out why the participants in the diet group of the WHI trial should be glad that they did not lower their fat intake any more than what they did!
Why the Low-Fat Diet is a Big Fat Fraud
One of the first priorities of healthy eating is to consume the most nutrient-dense foods possible. Cutting your fat intake strongly impedes this goal via at least three mechanisms:
1) Directly slashing your intake of important vitamins and fatty acids;
2) Reducing the absorption of crucial fat-soluble vitamins;
3) Decreasing the absorption of important minerals.
You probably think you're being "enlightened" when you trim the fat from your meats and ditch your egg yolks down the sink. What you are really doing is lucidly demonstrating what a mindless, brainwashed dolt you've become. You are effectively throwing away nutrients that your body needs to survive and thrive!
The fatty portions of meat, dairy and eggs are where one finds the highest concentrations of fat-soluble vitamins such as A, D, E and beta-carotene. Stripping the skin from your chicken breast not only makes it less tasty, but reduces its vitamin A content by seventy-eight percent!(1)
Throwing away your egg yolks is equally dumb. While one large egg yolk contains 245 IU of vitamin A, 18 IU of vitamin D, and 186 mcg of lutein plus zeaxanthin, along with small amounts of other carotenoids and vitamin E, a large egg white contains none of these nutrients. Egg yolks, along with beef liver, are also an especially concentrated dietary source of phosphatidylcholine (lecithin) and choline, which the body requires for healthy liver function and for the formation of the key neurotransmitter acetylcholine. Lower levels of acetylcholine are associated with memory loss and cognitive decline(2).
The last time you chose skim milk yogurt instead of the whole milk variety, you nutritionally short-changed yourself; skim yogurt contains 93 percent less vitamin A than whole yogurt! And if you chose non-fat yogurt, then congratulations--you received no vitamin A whatsoever!(1)
Data from national nutrition surveys consistently show that American children have lower than recommended intakes of vitamin E, and this is reflected in below-average serum levels of the vitamin. Reduction in dietary fat further exacerbates the low vitamin E status of children(3). The consequences of low dietary vitamin E intakes may include impaired immune responses, and an increased susceptibility to cardiovascular disease and cancer.
Willingly reducing your consumption of important vitamins and carotenes is not smart--it's downright stupid!
Absorb This!
Low-fat eating doesn't just decrease your intake of certain crucial nutrients. As researchers have shown time and time again, it will also dramatically reduce the absorption of whatever fat-soluble vitamins and carotenes remain in your diet!(4-7).
When subjects ingested equal amounts of lutein--a carotenoid that may protect against age-related macular degeneration and cataract--from either whole eggs, spinach or supplements, it was observed that lutein absorption was significantly higher during the period of whole egg consumption(8).
In another study, researchers compared the absorption of carotenoids from salads that contained either 0, 6 or 28 grams of canola oil. There was no increase in blood carotenoid concentrations after the fat-free salad, while the reduced fat salad produced markedly lower blood carotenoid elevations than the high fat version(9).
The addition of 150 grams of fat-rich avocado to salsa enhanced lycopene and beta-carotene absorption by 4.4 and 2.6-fold, respectively, compared to avocado-free salsa. In the same subjects, adding either twenty-four grams of avocado oil or 150 grams avocado to salad greatly enhanced alpha-carotene, beta -carotene and lutein absorption by 7.2, 15.3 and 5.1 times, respectively, compared with avocado-free salad!(10)
Only a true dumbass would think that reducing absorption of healthful fat-soluble nutrients is somehow beneficial. Don't be a dumbass.
Making a Bad Situation Worse
The mineral status of the typical Westerner is atrocious. Take magnesium for example, a substance vital for healthy heart function, blood sugar control, bone formation, and muscular contraction(11-16). A recent survey of U.S. adults found that the average daily intake of magnesium among Caucasian men is only 352 milligrams, and a mere 278 milligrams among African American men. Caucasian women consume an average of 256 milligrams per day, while African American women take in only 202 milligrams daily(17). The lower amounts of magnesium ingested by African Americans have been posited as a possible contributor to their increased susceptibility of hypertension, diabetes, and cardiovascular disease(18).
The situation isn't much better for zinc. Overt zinc deficiencies are common to Third World countries where animal protein consumption is low, while milder, 'sub-clinical' zinc deficiencies appear to be common in modernized nations. Nationwide food consumption surveys by the USDA have found that the average intake of zinc for males and females of all ages is below the recommended daily allowance (RDA). This is especially worrying when one considers that RDAs are generally based on the amount of a nutrient required to prevent obvious, well-recognized deficiency diseases (such as stunted growth and hypogonadism in the case of zinc), not sub-clinical deficiencies that may damage one's health over the longer-term.
Those who follow low fat diets are at even greater risk of zinc deficiency(19,20). Not only do low-fat diets discourage the consumption of zinc-rich foods like red meat, but a low dietary fat intake itself acts to impair mineral absorption.
It's ironic that red meat is typically denigrated for its saturated fat content, because saturates are the very fats that improve mineral absorption!(21-24).
A pilot study by researchers at the USDA Grand Forks Human Nutrition Research Center examined the effect of different fats and carbohydrate on performance and mineral metabolism in three male endurance cyclists. During alternating four-week periods, each subject consumed diets in which either carbohydrate, polyunsaturated, or saturated fat contributed about fifty percent of daily energy intake. Endurance capacity decreased with the polyunsaturated fat diet. The polyunsaturated diet also resulted in increased excretion of zinc and iron, while copper retention tended to be positive only on the saturated fat diet(25).
Optimal health is next to impossible to achieve with sub-optimal mineral status. Low-fat diets, most notably those low in saturated fats, encourage sub-optimal mineral status. Yet another reason why these diets suck the salsiccia, big time!
Low-Fat, Low Omega-3
Unless you've been living on a distant planet for the last few years, then you have no doubt heard about omega-3 fats and their pivotal role in maintaining good health.
Unlike low-fat diets, clinical trials utilizing the sole intervention of increased fatty fish or fish oil intake have produced significant reductions in CHD and overall mortality. The benefits of EPA and DHA-rich items like fish and fish oil are not confined to the cardiovascular system. In epidemiological studies and animal experiments, increased intakes of long-chain omega-3 fatty acids have been associated with lower rates of cancer, depression and mental illness, adverse pregnancy outcomes, infectious disease, osteoporosis, lung disease, menstrual pain, cognitive decline in the elderly, eye damage, childhood asthma and attention-deficit hyperactivity disorder(26-51). In clinical trials with human subjects, researchers have observed benefits from long-chain omega-3 supplementation in the treatment of asthma, alzheimers, rheumatoid arthritis, depression, schizophrenia, infant health, pregnancy outcomes, kidney disease, menstrual problems, ulcerative colitis, Crohn's disease and cystic fibrosis(52-73). Hell, even the fat-hating vegetarian Dean Ornish recommends the use of distinctly non-vegetarian fish oil supplements! (Gee, can anyone see a contradiction there?)
So what has this all got to do with low-fat eating? Everything!
Similar to fat-soluble vitamins, the absorption of EPA and DHA increases when consumed with a high fat meal(74).
Again, not just any old fat will do when it comes to improving one's omega-3 status. Saturated fat improves the body's conversion of plant-source omega-3 fats into the longer-chain varieties EPA and DHA, while omega-6-rich fats impede the conversion process. In young males, elongation of alpha-linolenic acid (ALA) and linoleic acid (LA) to DHA, EPA and AA was reduced by forty to fifty percent when dietary LA intake increased from fifteen to thirty grams per day(75).
When rats were supplemented with linseed oil, their serum and tissue content of the all-important omega-3 fatty acids increased, and omega-6 levels decreased, to a far greater extent on a saturated fat-rich (beef fat) diet than on a linoleic acid-rich (safflower oil) diet(76).
Cutting fat--as in saturated fat--worsens your omega-3 status. If you think that's a good thing, then low-fat nutrition has already scrambled your brain. My advice: Eat some fat before you become totally brain dead!
Speaking of scrambled brains…
Nature's Anti-Depressant: Fat!
Feeling moody? Irritable? Always snapping at your kids for no good reason? Are you known around the office as "Attila the Grump"? If so, eating a low-fat diet isn't going to help the situation. In fact, a low-fat diet may actually be the cause of your mental funk!
In 1998, U.K. researchers reported the results of an important experiment involving twenty healthy male and female volunteers. One group was placed on a 41% fat diet, while the other group consumed a 25% fat diet. After 4 weeks had passed, the groups were swapped around so that those originally on the low-fat diet were now consuming the high-fat diet, and vice-versa. Throughout the study, all meals were prepared by the university conducting the study and supplied to the participants. Both diets were specially designed to be as palatable and similar in taste as possible.
At the beginning and end of each diet period, every subject underwent a battery of psychological assessments, including various mood state questionnaires and an interview by a psychiatrist who was blinded to the participant's dietary status.
The study was tightly-controlled and adherence to the diets appears to have been high. HDL cholesterol levels declined during the low-fat period, a typical response on low-fat, high-carb diets, indicating that subjects ate the foods as supplied.
The researchers found that, while ratings of anger-hostility slightly declined during the high-fat diet period, they significantly increased during the low-fat, high-carb diet period!
Tension-anxiety ratings declined during the high-fat period, but did not change during the four weeks of low-fat, high-carb eating.
Ratings of depression declined slightly during the high-fat period, but increased during the low-fat, high-carb period, mainly due to two of the low-fat subjects reporting significantly greater depression-dejection ratings.
What is particularly alarming about this study is that the low-fat diet produced these symptoms in mentally healthy subjects. As the researchers emphasized, the participants were "a psychologically robust group who had never previously suffered from depression or anxiety, and who were not going through any 'stressful' events during the study." They further stated that "The alterations in mood observed in the present study may have been greater if subjects were feeling more stressed or were more susceptible to mental illness."(77)
Low-fat diets should be approached with extreme caution by those with a history of depression, anxiety, overly aggressive behavior or mental illness. Such individuals may be especially vulnerable to the nutritional inadequacies of low-fat diets.
The UK researchers' observations raise some interesting questions. Could the low-fat, high-carbohydrate diets that have been so heavily promoted over the last thirty years be at least partially responsible for increases in anti-social behavior witnessed during the same period? If studies with our primate cousins are anything to go by, the answer to this question could well be affirmative.
Low-Fat Diet Makes Monkeys Go Ape
For almost 2 years, adult male monkeys were fed a "luxury" diet - (43% calories from fat, 0.34 mg cholesterol/Calorie of diet) or a "prudent" diet (30% calories from fat, 0.05 mg cholesterol/Calorie of diet).
Researchers observed that the low-fat diet monkeys were more irritable and initiated more aggression than the "luxury" diet animals.
The prudent diet resulted in lower total serum cholesterol levels, something that our absent-minded health authorities automatically assume is a good thing. The researchers, however, noted: "These results are consistent with studies linking relatively low serum cholesterol concentrations to violent or antisocial behavior in psychiatric and criminal populations and could be relevant to understanding the significant increase in violence-related mortality observed among people assigned to cholesterol-lowering treatment in clinical trials."(78)
Fatless Shrugged
It was Ayn Rand who once said that the most noble and productive goal for a person to engage in was the pursuit of their own happiness. If the achievement of your own happiness is important to you, then kick the low-fat diet's sad, sorry, melancholy butt right out of your life--it's a loser. Low-Fat Diets Lower Testosterone
Testosterone is abhorred by politically correct weenies, who like to blame it for every instance of disagreeable male behavior, in much the same way menstruation was once cited as the catch-all explanation for uncharacteristically aggressive or irritable female behavior.
Of course, scientific reality is of little concern to the politically correct. The fact is, testosterone is an extremely important hormone for both men and women. Sex drive, muscle and bone health, immune function, cognitive function, mood, and cardiovascular health are all negatively affected by declining levels of testosterone. Testosterone levels typically decline with age, and, along with the decline of other key hormones, falling T levels are believed to be a major contributor to many of the deleterious changes seen during the aging process. As such, aging individuals should be looking at ways to preserve and even boost their testosterone status, rather than engaging in self-defeating habits that will speed the decline in T levels. Alcohol abuse, recreational drug use, pharmaceutical drugs, stress, and poor sleep habits can all lower testosterone levels.
So too can low-fat diets.
Research shows that reducing fat intake from around forty percent to 20-25 percent of calories decreases testosterone output. Low fat diets also increase levels of sex hormone-binding globulin (SHBG), a protein which binds to testosterone, thus reducing the amount of bioavailable, or 'free', testosterone in the body. It is free testosterone that is responsible for this hormone's favorable effects on growth, repair, sexual capacity and immune function(79-81).
Again, not just any old fat will suffice when it comes to optimizing testosterone levels. A study with weight-training men showed higher saturated fat and monounsaturated fat consumption to be positively associated with testosterone levels. In contrast, higher dietary levels of so-called "heart-healthy" polyunsaturated fats relative to saturated fats were associated with lower testosterone levels (82).
It's highly ironic that athletes and bodybuilders will take all manner of expensive, esoteric and often dubious testosterone-boosting concoctions--not to mention anabolic steroids--yet will follow hormone-damping low-fat diets with religious fervor. It's a little like putting on a weighted vest before a big race and expecting to run at full speed.
Hormones like testosterone play a fundamentally important role in stimulating and regulating growth and metabolism. Don't go throwing a low-fat monkey wrench into your metabolic engine!
Low-Fat Diets and Immune FunctionDiet 'experts' assure us that a low-fat diet is the key to good health. The published research does not support such claims.
Despite the virulent ranting of anti-fat activists, trials comparing sedentary adult volunteers fed low-fat diets with those receiving higher fat diets has shown no improvement in immune status in the former group(83,84).
In children, whole milk consumption is associated with fewer gastrointestinal infections than consumption of low fat milk (85). Rats consuming diets high in milk fat show a significantly greater resistance to Listeria infection and higher survival rates than those whose diets were low in milk fat(86). Similar results have been observed in mice fed diets high in saturate-rich coconut oil(87)
In athletes, who are constantly pushing their immune systems to the edge with strenuous training, adherence to the commonly-recommended low-fat high-carbohydrate diet (15-19% of total calories) increases pro-inflammatory immune factors, decreases anti-inflammatory factors, and depresses antioxidant status when compared to higher fat diets (30-50% of total calories)(88,89). Such changes may leave athletes on low-fat diets with a lowered resistance to infection and a higher risk of chronic illness. This may be due to difficulty in obtaining sufficient calories from low-fat diets to meet the energy demands of exercise; increasing dietary fat intake and total caloric intake to match energy expenditure appears to reverse the negative effects on immune function reported on calorie-deficient, low-fat diets. Diets comprising 32% to 55% fat also improve endurance capacity compared to diets with 15% fat(90).
It was Scandinavian researchers who, in the 1960s, performed research showing that using extremely high-carbohydrate, low-fat diets for short periods could enhance athletic performance. This was achieved by using these diets as part of a "depletion-repletion" carbohydrate-loading strategy, which helped temporarily elevate muscle glycogen stores to higher than usual levels. One of the pioneers in this area, Dr. Jan Karlsson, points out that such diets were never intended to be applied for more than 3-4 days. Karlsson and his colleagues openly lament that these diets are now employed for extended periods of time, and refer to the prolonged use of very high-carbohydrate/low-fat diets by athletes as "voluntary malnourishment". They note that in Scandinavia, researchers use the term "Carbohydrate Trap" when referring to the widespread belief that these diets are required for optimal performance. These researchers consider a 50-55% carbohydrate, 35% fat diet to be eminently more sensible and nutritious than the >60% carb, <25% fat diets commonly used by athletes(91).
For athletes and non-athletes alike, the low-fat diet is a sick (pun intended) joke.
The Low-Fat Diet Does Not Protect Against Heart Disease, and May Actually Worsen It
The WHI trial confirmed what well-read cholesterol skeptics have known for a long time: The low-fat diet is a big fat fraud when it comes to preventing heart disease. Among the 48,835 women participating in the trial, no significant differences in CHD or stroke incidence, CHD or stroke mortality, or total mortality were observed(92). Nor were there any reductions in the incidence or mortality rates of breast cancer, colorectal cancer, or total cancer(93,94).
There was however, one very ominous finding to emerge from the WHI trial. Among the 3.4 percent of trial participants with pre-existing cardiovascular disease, those randomized to the low-fat diet experienced a 26% increase in the relative risk of non-fatal and fatal CHD!
Low-fat advocates have remained deafeningly silent on this inconvenient finding, and would no doubt like to believe this was just a 'freak' occurrence. However, this is hardly the first time that low-fat eating has been shown to worsen the prognosis of women with existing cardiovascular disease.
In 2004, the world's most prominent nutrition journal, The American Journal of Clinical Nutrition, published the results of a very, very interesting study. Harvard researchers had taken 235 postmenopausal women with established coronary heart disease, and divided them into four categories according to their level of saturated fat intake. They then performed coronary angiographies at baseline and after a mean follow-up of 3.1 years, analyzing over 2,200 coronary artery segments in the process.
After adjusting for multiple confounders, a higher saturated fat intake was associated with less narrowing of the arteries and less progression of coronary atherosclerosis. Compared with a 0.22 mm narrowing in the lowest quartile of intake, there was a 0.10-mm narrowing in the second quartile, a 0.07 mm narrowing in the third quartile, and no narrowing in the fourth and highest quartile of saturated fat intake!
Following a low-fat diet means adopting a high-carbohydrate diet by default. After all, it is exceedingly difficult and highly unpalatable to achieve the bulk of one's caloric needs by eating lean protein foods. It is of no small concern then, that carbohydrate intake was positively associated with atherosclerotic progression, particularly when the glycemic index was high. The intake of so-called 'heart-healthy' polyunsaturated fats was also positively associated with progression of atherosclerosis, but monounsaturated and total fat intakes were not associated with progression (it must be noted that the major sources of polyunsaturates in Western countries are refined vegetable oils which are rich in the omega-6 fat linoleic acid. The polyunsaturated omega-3 fats, which are underconsumed by most Westerners, have actually been shown to lower CVD).
After examining the baseline data for the study subjects, it is apparent that the results can not be explained away by otherwise healthier lifestyles among those eating the most saturated fat; the high saturated fat group, in fact, had the greatest number of current smokers! Women eating the most saturated fat were also less likely to take blood-thinning medications like aspirin(95).
If this study had found saturated fats to be associated with cardiovascular disease, its results would have been trumpeted in headlines around the world. Instead, they were largely ignored by the mainstream media and our ever-so responsible 'health' authorities. It appears only studies that support the cherished dogma of our health orthodoxy are considered suitable as press release fodder…
A major factor in the progression of cardiovascular disease--and most major diseases--is free radical damage. It is well-established that saturated fatty acids, because of their lack of vulnerable double bonds, are the least susceptible to free radical damage; polyunsaturates are the most vulnerable. We also know that increased carbohydrate consumption, especially of the refined variety, does an outstanding job of raising blood sugar and insulin levels, which accelerates glycation, free radical activity, blood clot formation, and arterial smooth muscle cell proliferation.
It should also be noted that increasing heart disease incidence throughout the twentieth century has been accompanied by increasing polyunsaturate consumption, while a marked increase in refined carbohydrate consumption during the last three decades has been accompanied by spiralling obesity and diabetes incidence. Animal fat consumption, in contrast, has remained stable over the last 100 years.
So what we have is two studies that show that women with pre-existing heart disease will experience WORSE outcomes if they shun saturated fat and opt for a low-fat/high-carbohydrate diet! Furthermore, the validity of these results is supported by basic biochemistry and epidemiological data. So will low-fat advocates stop recommending this pattern of eating to women with heart disease? Does their concern for human life override their need to defend their precious low-fat dogma at all costs?
I truly doubt it…
If low-fat advocates won't be straight with you, then I will. Let's be perfectly clear on this: If you are female, and suffer cardiovascular disease, the published, peer-reviewed scientific evidence indicates that adopting a low-fat diet could be DEADLY.
The WHI is not the only dietary intervention trial to demonstrate the worthlessness of the low-fat diet in preventing CVD. In 1965, the prominent journal Lancet published the results of a trial conducted by the UK Medical Research Committee. In this study, 264 men under 65 were assigned to either a low-fat diet or their usual diet. Dietary records show that those in the low-fat group averaged 45 g/day of fat throughout the trial, while those in the control group actually increased their average fat intake from 106 to 125g. The average serum cholesterol measurement of the low-fat group was 25 points lower than that of the control group at 4 years. Despite nonsensical claims that "every 1mg'dl drop in cholesterol equals a 2% drop in CHD risk", there were no differences between the two groups in CHD incidence or mortality after 4 years.
In Search of the Elusive 'Negative Fat Intake'!
The hysterical anti-fat vitriole that spews forth from some anti-fat faddists leads me to believe that if these clowns could eat a 'negative-fat' diet, they would! As for their argument that the above trials didn't lower fat enough, one has to wonder how creating even greater deficiencies in valuable nutrients, and predisposing one to greater risk of depression and anger--all of which low-fat diets have indeed been clinically documented to do--will in any way help prevent heart disease! Maybe these folks have been eating low-fat so long that it's started to drain their brains; healthy human brains, after all, are 60% fat by weight!
The authors of the MRC trial concluded that: "A low-fat diet has no place in the treatment of myocardial infarction." Despite being written over forty years ago, these words have largely been ignored by a medical and health hierarchy which seems to earnestly believe that if only it keeps flogging the dead low-fat horse, it will one-day magically spring to life. In Australia, this is known as engaging in a 'wank', which means that people who push low-fat diets despite no proof whatsoever of their efficacy are wankers. This might be stating the obvious, but…you really shouldn't listen to wankers!
But the Japanese Eat a Low-Fat Diet…Don't They?
Supporters of low-fat nutrition cite the Japanese ad nauseum, claiming that their low-fat/high-carbohydrate diet is the reason for their low rate of heart disease. It is ironic that many of these same commentators exhort the benefits of whole-grains and tell us that the only 'bad' carbohydrates are those that come from refined sugars and grains. These folks need to get their story straight---a major source of carbohydrates in the Japanese diet is white rice--a refined grain! That means that if the high-carbohydrate Japanese diet is cardio-protective, then refined grains must be good for one's heart! Well, which is it? You can have it both ways; either refined grains are heart-friendly, or they're not!
The truth is, the longevity and low CHD incidence of the Japanese owes nothing to carbohydrate intake, refined or otherwise. During the 1960s and 1970s, industrialization underwent rapid growth in Japan. This period of marked economic change bought with it greater consumption of animal protein and fat. This increased animal food consumption in Japan has been accompanied by a marked decline in both the overall incidence of and the mortality from one of that nation's biggest killers--stroke. This increase in animal protein and animal fat consumption has also occurred alongside Japan's rise to the top of the longevity ladder.(96,97)
If you're tempted to write this off as merely a consequence of improved living standards and medical technology, keep in mind that long-term follow-up studies with both native and migrant Japanese populations show that those who eat the most animal protein and animal fat enjoy greater longevity and a lower incidence of stroke than those who eat lesser amounts(98-101).
OK, So What About the Mediterranean Diet?
A diet low in saturated fat is purportedly a major factor in the low rates of CHD observed in Southern European countries. Just one wee problem: France, the Mediterranean country with the lowest CHD rates of all, is also the Mediterranean country with the highest saturated fat intake!
Oops!
Health 'experts' have tried to brush off this embarrassing observation as a 'paradox' (orthodoxy loves applying the 'paradox' label to uncomfortable contradictions) by claiming that red wine explains this difference. If that were true, then the Italians, who drink a similar amount of red wine, should have CHD rates even lower than France. But they don't; their CHD rates are similar to those of other Southern European countries where far less red wine is consumed(102).
Conclusion
I could go on, and on, and on…but I'll just close by saying that the low-fat diet has NEVER been demonstrated to do all the wonderful health-fortifying things claimed for it. The only trials showing favorable effects in people following low-fat diets are those that simultaneously employed other truly useful interventions, like exercise, stress management, increased fruit and vegetable intake and decreased processed food intake, and weight loss. However, there is absolutely no law whatsoever stating that low-fat eating is required for the implementation of any of these strategies. In fact, given the available evidence, one can only conclude that the inclusion of higher fat intakes in these trials may even have improved the results!
The bottom line: Not only is low-fat eating a boring way to go through life, it is a useless and often counterproductive hoax.
References and Assorted Disclaimers:
DISGRUNTLED WORSHIPPERS OF THE LOW-FAT RELIGION SHOULD READ THE FOLLOWING:I have not stated anything in this article that cannot be verified by published, peer-reviewed research. Nonetheless, my inbox will no doubt be flooded with angry emails from those who have been brainwashed by the low-fat paradigm, and who violently object to the thought that something that they have believed in so strongly for so long might actually be false. In other words, malevolent dimwits who want to shoot the messenger! For those of you who fall into this category, my suggestions are as follows: 1) GROW UP!; 2) Start placing a premium on discovering the facts, as opposed to doggedly defending what you have already decided you want to believe; 3) Instead of attacking me, start questioning the motives of those who profit greatly from the fallacious anti-fat, anti-cholesterol paradigm. This includes the food and drug conglomerates that make BILLIONS from the sale of low-fat foods and cholesterol-lowering drugs, the health and dietetic 'associations/organizations/institutes/foundations/etc' who receive millions in 'donations' from these very same companies, and the executives of these so-called 'non-profit' organizations who enjoy six-figure incomes and extensive perquisites.
To attack the owner of a non-commercial web site, who has nothing to gain financially by either supporting or opposing the low-fat paradigm, and defending those WHO DO, is so bloody stupid that it defies comprehension. Unfortunately, there are a lot of bloody stupid people in the world! If you are one of them, and decide to write me, please note that unless your email contains valid references to the scientific literature, it will be deleted immediately. After having established yourself as an ignorant goofball, your email address will also be added to my spam filter and any further emails will be delivered straight to my trash. Sorry, but I really am extremely busy and have no time or patience for ignorant, time-wasting twits.
NOTE: I have no problem with people reprinting this article on other web sites for non-commercial purposes. Heck, you can post it on the side of the Empire State Building for all I care (just be sure to seek permission from the owners first). However, PLEASE ENSURE that you give full credit to the author, whether you reproduce the article in whole or part. A hyperlink to www.TheOmnivore.com would also be greatly appreciated! Those wishing to reprint this or any other article on TheOmnivore.com for commercial purposes should email: ac.theomnivore@gmail.com
References
1. USDA National Nutrient Database for Standard Reference. Available online: http://www.nal.usda.gov/fnic/foodcomp/search/
2. Giacobini E. Cholinergic function and Alzheimer's disease. Int J Geriatr Psychiatry. 2003 Sep; 18 (Suppl 1): S1-S5.
3. Bendich A. Vitamin E status of US children. Journal of the American College of Nutrition, Aug, 1992; 11 (4): 441-444.
4. Takyi EE. Children's consumption of dark green, leafy vegetables with added fat enhances serum retinol. Journal of Nutrition, 1999; 129 (8): 1549-1554.
5. Jalal F, et al. Serum retinol concentrations are affected by food sources of ß-carotene, fat intake, and anthehelmintic drug treatment. American Journal of Clinical Nutrition, 1998; 68: 623-629.
6. Roodenburg JA, et al. Amount of fat in the diet affects bioavailability of lutein esters but not of {alpha}-carotene, {beta}-carotene, and vitamin E in humans. American Journal of Clinical Nutrition, 2000; 71 (5): 1187-1193.
7. Drammeh BS, et al. A Randomized, 4-Month Mango and Fat Supplementation Trial Improved Vitamin A Status among Young Gambian Children. Journal of Nutrition, 2002; 132 (12): 3693 - 3699.
8. Chung H-Y, et al. Lutein Bioavailability Is Higher from Lutein-Enriched Eggs than from Supplements and Spinach in Men. Journal of Nutrition, 2004; 134: 1887-1893.
9. Brown MJ, et al. Carotenoid bioavailability is higher from salads ingested with full-fat than with fat-reduced salad dressings as measured with electrochemical detection. American Journal of Clinical Nutrition, Aug. 2004; 80: 396-403.
10. Unlu NZ, et al. Carotenoid Absorption from Salad and Salsa by Humans Is Enhanced by the Addition of Avocado or Avocado Oil. Journal of Nutrition, Mar, 2005; 135: 431-436.
11. Fox C, et al. Magnesium: its proven and potential clinical significance. Southern Medical Journal, Dec, 2001; 94 (12): 1195-1201.
12. Shechter M, et al. Effects of oral magnesium therapy on exercise tolerance, exercise-induced chest pain, and quality of life in patients with coronary artery disease. American Journal of Cardiology, Mar 1, 2003; 91 (5): 517-521.
13. Shechter M, et al. Beneficial antithrombotic effects of the association of pharmacological oral magnesium therapy with aspirin in coronary heart disease patients. Magnesium Research, Dec, 2000; 13 (4): 275-284.
14. Shechter M, et al. Oral magnesium therapy improves endothelial function in patients with coronary artery disease. Circulation, Nov 7, 2000; 102 (19): 2353-2358.
15. Guerrero-Romero F, et al. Oral magnesium supplementation improves insulin sensitivity in non-diabetic subjects with insulin resistance. A double-blind placebo-controlled randomized trial. Diabetes & Metabolism, Jun, 2004; 30 (3): 253-258.
16. Rodriguez-Moran M, Guerrero-Romero F. Oral magnesium supplementation improves insulin sensitivity and metabolic control in type 2 diabetic subjects: a randomized double-blind controlled trial. Diabetes Care, Apr, 2003; 26 (4): 1147-1152.
17. Ford ES, Mokdad, AH. Dietary Magnesium Intake in a National Sample of U.S. Adults. Journal of Nutrition, 2003; 133: 2879-2882.
18. Fox CH, et al. Magnesium deficiency in African-Americans: does it contribute to increased cardiovascular risk factors? Journal of the National Medical Association, 2003 Apr; 95 (4): 257-62.
19. Retzlaff BM, et al. Changes in vitamin and mineral intakes and serum concentrations among free-living men on cholesterol-lowering diets: the Dietary Alternatives Study. American Journal of Clinical Nutrition, 1991; 53 (4): 890-898.
20. Baghurst KI, et al. Demographic and dietary profiles of high and low fat consumers in Australia. Journal of Epidemiology and Community Health, 1994; 48 (1): 26-32.
21. Mahoney AW, et al. Effects of level and source of dietary fat on the bioavailability of iron from turkey meat for the anemic rat. Journal of Nutrition, 1980: 110 (8): 1703-1708.
22. Johnson PE, et al. The effects of stearic acid and beef tallow on iron utilization by the rat. Proc Soc Exp Biol Med, 1992; 200 (4): 480-486.
23. Koo SI, Ramlet JS. Effect of dietary linoleic acid on the tissue levels of zinc and copper, and serum high-density lipoprotein cholesterol. Atherosclerosis, 1984; 50 (2): 123-132.
24. Van Dokkum W, et al. Effect of variations in fat and linoleic acid intake on the calcium, magnesium and iron balance of young men. Ann Nutr Metab, 1983; 27 (5): 361-369.
25. Lukaski HC, et al. Interactions among dietary fat, mineral status, and performance of endurance athletes: a case study. Int J Sport Nutr Exerc Metab, Jun 2001; 11 (2): 186-198.
26. Ip, et al. Requirement of essential fatty acid for mammary tumorigenesis in the rat. Cancer Research, 1985; 45 (5): 1997-2001.
27. Rose DP. Effects of dietary fatty acids on breast and prostate cancers: evidence from in vitro experiments and animal studies. American Journal of Clinical Nutrition, Dec, 1997; 66 (6 Suppl): 1513S-1522S.
28. Fernandez E, et al. Fish consumption and cancer risk. American Journal of Clinical Nutrition, Jul 1, 1999; 70(1): 85-90.
29. Terry P, et al. Fatty fish consumption and risk of prostate cancer. Lancet, Jun 2, 2001; 357 (9270): 1764-1766.
30. Terry P, et al. Fatty fish consumption lowers the risk of endometrial cancer: a nationwide case-control study in Sweden. Cancer Epidemiology, Biomarkers & Prevention, Jan, 2002; 11 (1): 143-145.
31. Maillard V, et al. N-3 and N-6 fatty acids in breast adipose tissue and relative risk of breast cancer in a case-control study in Tours, France. International Journal of Cancer, Mar 1, 2002; 98 (1): 78-83.
32. Kato I, et al. Prospective study of diet and female colorectal cancer: the New York University Women's Health Study. Nutrition and Cancer, 1997; 28: 276-281.
33. Hakim IA, et al. Fat intake and risk of squamous cell carcinoma of the skin. Nutrition and Cancer, 2000; 36 (2): 155-162.
34. Tanskanen A, et al. Fish Consumption and Depressive Symptoms in the General Population in Finland. Psychiatric Services, Apr, 2001; 52: 529-531.
35. Adams PB, et al. Arachidonic acid to eicosapentaenoic acid ratio in blood correlates positively with clinical symptoms of depression. Lipids, Mar, 1996; 31 (Suppl): S157-161.
36. Mamalakis G, et al. Depression and adipose essential polyunsaturated fatty acids. Prostaglandins, Leukotrienes, and Essential Fatty Acids, Nov, 2002; 67 (5): 311-318.
37. Laugharne JD, et al. Fatty acids and schizophrenia. Lipids, Mar, 1996; 31 (Suppl): S163-165.
38. Olsen SF, Secher NJ. Low consumption of seafood in early pregnancy as a risk factor for preterm delivery: prospective cohort study. British Medical Journal, Feb 23, 2002; 324: 447.
39. Williams MA, et al. Omega-3 fatty acids in maternal erythrocytes and risk of preeclampsia. Epidemiology, May, 1995; 6 (3): 232-237.
40. Hibbeln JR. Seafood consumption, the DHA content of mothers' milk and prevalence rates of postpartum depression: a cross-national, ecological analysis. Journal of Affective Disorders, May, 2002; 69(1-3): 15-29.
41. Turek JJ, et al. Dietary polyunsaturated fatty acids modulate responses of pigs to Mycoplasma hyopneumoniae infection. Journal of Nutrition, Jun, 1996; 126 (6): 1541-1548.
42. Tully AM, et al. Low serum cholesteryl ester-docosahexaenoic acid levels in Alzheimer's disease: a case-control study. British Journal of Nutrition, Apr, 2003; 89 (4): 483-489.
43. Requirand P, et al. Serum fatty acid imbalance in bone loss: example with periodontal disease. Clinical Nutrition, Aug, 2000; 19 (4): 271-276.
44. Watkins BA, et al. Nutraceutical Fatty Acids as Biochemical and Molecular Modulators of Skeletal Biology. Journal of the American College of Nutrition, 2001; 20 (90005): 410S-416S.
45. Reinwald S, et al. Repletion with (n-3) Fatty Acids Reverses Bone Structural Deficits in (n-3)-Deficient Rats. Journal of Nutrition, Feb 2004; 134: 388-394.
46. Schwartz J. Role of polyunsaturated fatty acids in lung disease. American Journal of Clinical Nutrition, Jan 2000; 71 (suppl): 393S-96S.
47. Shahar E, et al. Dietary n-3 polyunsaturated fatty acids and smoking-related chronic obstructive pulmonary disease. New England Journal of Medicine, Jul 28, 1994: 331 (4): 228-233.
48. Deutch B. Menstrual pain in Danish women correlated with low n-3 polyunsaturated fatty acid intake. European Journal of Clinical Nutrition, 1995; 49: 508-516.
49. Kalmijn, S., et al. Polyunsaturated fatty acids, antioxidants, and cognitive function in very old men. American Journal of Epidemiology, Jan 1, 1997: 145: 33-41.
50. Seddon JM, et al. Dietary Fat and Risk for Advanced Age-Related Macular Degeneration. Archives of Ophthalmology, 2001; 119 (8): 1191-1199.
51. Hodge L, et al. Consumption of oily fish and childhood asthma risk. Medical Journal of Australia, 1996; 164: 137-140.
52. Dry J, Vincent D. Effect of a fish oil diet on asthma: results of a 1-year double-blind study. International Archives of Allergy and Applied Immunology, 1991; 95 (2/3): 156-157.
53. Burgess JR, et al. Long-chain polyunsaturated fatty acids in children with attention-deficit hyperactivity disorder. American Journal of Clinical Nutrition, 2000; 71: 327-330.
54. Yehuda S, et al. Essential fatty acids preparation (SR-3) improves Alzheimer's patients quality of life. International Journal of Neuroscience, Nov, 1996; 87 (3-4): 141-149.
55. Geusens P et al. Long-term effect of omega-3 fatty acid supplementation in active rheumatoid arthritis, a 12-month, double-blind, controlled study. Arthritis & Rheumatism, Jun, 1994; 37 (6): 824-829.
56. Schiz Peet M, Horrobin DF. A dose-ranging study of the effects of ethyl-eicosapentaenoate in patients with ongoing depression despite apparently adequate treatment with standard drugs. Archives of General Psychiatry, Oct, 2002; 59 (10): 913-919.
57. Stoll AL, et al. Omega 3 fatty acids in bipolar disorder: a preliminary double-blind, placebo-controlled trial. Archives of General Psychiatry, May, 1999; 56 (5): 407-412.
58. Peet M, et al. Two double-blind placebo-controlled pilot studies of eicosapentaenoic acid in the treatment of schizophrenia. Schizophrenia Research, Apr 30, 2001; 49 (3): 243-251.
59. Peet M, Horrobin DF. A dose-ranging exploratory study of the effects of ethyl-eicosapentaenoate in patients with persistent schizophrenic symptoms. Journal of Psychiatric Research, Jan-Feb, 2002; 36 (1): 7-18.
60. Hamazaki T, et al. The Effect of Docosahexaenoic Acid on Aggression in Young Adults. A Placebo-controlled Double-blind Study. Journal of Clinical Investigation, Feb, 1996; 97 (4): 1129-1134.
61. Jorgensen MH, et al. Effect of formula supplemented with docosahexaenoic acid and gamma-linolenic acid on fatty acid status and visual acuity in term infants. Journal of Pediatric Gastroenterology and Nutrition, 1998; 26: 412-421.
62. Carlson SE, et al. Visual acuity and fatty acid status of term infants fed human milk and formulas with and without docosahexaenoate and arachidonate from egg yolk lecithin. Pediatric Research, 1996; 39: 882-888.
63. O'Connor DL, et al. Growth and Development in Preterm Infants Fed Long-Chain Polyunsaturated Fatty Acids: A Prospective, Randomized Controlled Trial. Pediatrics, Aug 1, 2001; 108 (2): 359-371.
64. Helland IB, et al. Maternal Supplementation With Very-Long-Chain n-3 Fatty Acids During Pregnancy and Lactation Augments Children's IQ at 4 Years of Age. Pediatrics, Jan, 2003; 111 (1): e39-e44.
65. Dunstan JA, et al. Fish oil supplementation in pregnancy modifies neonatal allergen-specific immune responses and clinical outcomes in infants at high risk of atopy: a randomized, controlled trial. Journal of Allergy and Clinical Immunology, Dec, 2003; 112 (6): 1178-1184.
66. Olsen SF, et al. Randomised controlled trial of effect of fish-oil supplementation on pregnancy duration. Lancet, Apr 25, 1992; 339 (8800): 1003-1007.
67. Olsen SF, Secher NJ. A possible preventive effect of low-dose fish oil on early delivery and pre-eclampsia: indications from a 50-year-old controlled trial. British Journal of Nutrition, Nov, 1990; 64 (3): 599-609.
68. De Caterina R et al. n-3 fatty acids and renal diseases. American Journal of Kidney Diseases, Sept, 1994; 24 (3): 397-415.
69. Harel Z et al. Supplementation with omega-3 polyunsaturated fatty acids in the management of dysmenorrhea in adolescents. American Journal of Obstetrics & Gynecology, Apr, 1996; 174 (4): 1335-1338.
70. Aslan A, Triadafilopoulos G. Fish oil fatty acid supplementation in active ulcerative colitis: A double-blind, placebo-controlled, crossover study. American Journal of Gastroenterology, Apr, 1992; 87: 432-37.
71. Salomon, P., et al. Treatment of ulcerative colitis with fish oil n-3 omega fatty acid: an open trial. Journal of Clinical Gastroenterology, Apr, 1990; (12): 157-1161.
72. Belluzzi A et al. Effect of an enteric-coated fish-oil preparation on relapses in Crohn's disease. New England Journal of Medicine, Jun 13, 1996; 334 (24): 1557-1560.
73. Lawrence R, Sorrell T. Eicosapentaenoic acid in cystic fibrosis: evidence of a pathogenetic role for leukotriene B4. Lancet, Aug 21, 1993; 342: 465-469.
74. Lawson LD, Hughes BG. Absorption of eicosapentaenoic acid and docosahexaenoic acid from fish oil triacylglycerols or fish oil ethyl esters co-ingested with a high-fat meal. Biochem Biophys Res Commun, Oct 31, 1988; 156 (2): 960-963.
75. Emken EA, et al. Dietary linoleic acid influences desaturation and acylation of deuterium-labeled linoleic and linolenic acids in young adult males. Biochim Biophys Acta, Aug 4, 1994; 1213 (3): 277-288.
76. Garg ML, et al. Dietary saturated fat level alters the competition between alpha-linolenic and linoleic acid. Lipids 1989 Apr;24(4): 334-339.
77. Wells AS, et al. Alterations in mood after changing to a low-fat diet. British Journal of Nutrition, Jan, 1998; 79 (1): 23-30.
78. Kaplan JR, et al. The effects of fat and cholesterol on social behavior in monkeys. Psychosom Med. 1991 Nov-Dec; 53 (6): 634-642.
79. Hamalainen EK, et al. Decrease of serum total and free testosterone during a low-fat high-fibre diet. J Steroid Biochem. Mar 1983; 18 (3): 369-370.
80. Reed MJ, et al. Dietary lipids: an additional regulator of plasma levels of sex hormone binding globulin. J. Clin. Endocrinol. Metab, 1987; 64: 1083-1085.
81. Dorgan JF, et al. Effects of dietary fat and fiber on plasma and urine androgens and estrogens in men: a controlled feeding study. Am J Clin Nutr. Dec 1996; 64 (6): 850-855.
82. Volek JS, et al. Testosterone and cortisol in relationship to dietary nutrients and resistance exercise. Journal of Applied Physiology, Jan 1997; 82 (1): 49-54.
83. Kelley DS, et al. Energy restriction decreases number of circulating natural killer cells and serum levels of immunoglobulins in overweight women. European Journal of Clinical Nutrition, Jan, 1994; 48 (1): 9-18.
84. van het Hof KH, et al. A long-term study on the effect of spontaneous consumption of reduced fat products as part of a normal diet on indicators of health. International Journal of Food Sciences and Nutrition, Jan, 1997; 48 (1): 19-29.
85. Koopman JS, et al. Milk fat and gastrointestinal illness. Am. J. Public Health 1984; 74: 1371-1373
86. Puertollano MA, et al. Relevance of Dietary Lipids as Modulators of Immune Functions in Cells Infected with Listeria monocytogenes. Clinical and Diagnostic Laboratory Immunology, Mar. 2002; 9 (2): 352-357.
87. de Pablo MA, et al. Determination of natural resistance of mice fed dietary lipids to experimental infection induced by Listeria monocytogenes. FEMS Immunol Med Microbiol. 2000 Feb;27(2):127-33.
88. Meksawan K, et al. Effect of dietary fat intake and exercise on inflammatory mediators of the immune system in sedentary men and women. Journal of the American College of Nutrition, Aug, 2004; 23 (4): 331-340.
89. Venkatraman JT, et al. Dietary fats and immune status in athletes: clinical implications. Medicine and Science in Sports and Exercise, Jul, 2000; 32 (7 Suppl): S389-S395.
90. Pendergast DR, et al. A perspective on fat intake in athletes. Journal of the American College of Nutrition, 2000 Jun; 19 (3): 345-350.
91. Göransson U, et al. The 'Are´ Sport Nutratherapy Program: The Rationale for Food Supplements in Sports Medicine. In: Simopoulos AP, Pavlou KN (eds). Nutrition and Fitness: Metabolic and Behavioral Aspects in Health and Disease. World Review of Nutrition and Dietetics, 1997; 82: 101-121.
92. Howard BV, et al. Low-Fat Dietary Pattern and Risk of Cardiovascular Disease: The Women's Health Initiative Randomized Controlled Dietary Modification Trial. Journal of the American Medical Association, Feb 8, 2006; 295: 655-666.
93. Prentice RL, et al. Low-Fat Dietary Pattern and Risk of Invasive Breast Cancer: The Women's Health Initiative Randomized Controlled Dietary Modification Trial. Journal of the American Medical Association, Feb 8, 2006; 295: 629-642.
94. Beresford SAA, et al. Low-Fat Dietary Pattern and Risk of Colorectal Cancer: The Women's Health Initiative Randomized Controlled Dietary Modification Trial. Journal of the American Medical Association, Feb 8, 2006; 295: 643-654.
95. Mozaffarian D, et al. Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. American Journal of Clinical Nutrition, 2004; 80: 1175-1184.
96. Tanaka H, et al. Secular trends in mortality for cerebrovascular disease in Japan, 1960-1979. Stroke, 1982; 13: 574-581.
97. Nakayama C, et al. A 15.5-Year Follow-up Study of Stroke in a Japanese Provincial City: The Shibata Study. Stroke, Jan 1, 1997; 28(1): 45-52.
98. Iso H, et al. Fat and protein intakes and risk of intraparenchymal hemorrhage among middle-aged Japanese. American Journal of Epidemiology, Jan 1, 2003; 157 (1): 32-39.
99. Abbott RD, et al. Effect of dietary calcium and milk consumption on risk of thromboembolic stroke in older middle-aged men: The Honolulu Heart Program. Stroke, May 1996; 27: 813 - 818.
100. Sauvaget C, et al. Intake of animal products and stroke mortality in the Hiroshima/Nagasaki Life Span Study. International Journal of Epidemiology, Aug 1, 2003; 32 (4): 536-543.
101. Sauvaget C, et al. Animal Protein, Animal Fat, and Cholesterol Intakes and Risk of Cerebral Infarction Mortality in the Adult Health Study. Stroke, 2004; 35: 1531.
102. Food intake data from Food and Agriculture Organization of the United Nations, Statistical Database. CHD mortality data from World Health Statistics Annual, 1961, 1966 and 1997-1999 editions.
Here is a quote from near the end of the article. "NOTE: I have no problem with people reprinting this article on other web sites for non-commercial purposes. Heck, you can post it on the side of the Empire State Building for all I care (just be sure to seek permission from the owners first). However, PLEASE ENSURE that you give full credit to the author, whether you reproduce the article in whole or part."
=====================================================
Why the Low-Fat Diet is Stupid and Potentially Dangerous
Anthony Colpo, February 23, 2006.
On February 8, 2006, the Journal of the American Medical Association delivered a huge blow to advocates of low-fat 'nutrition' by publishing the results of the huge Women's Health Initiative trial. The results of the trial clearly showed that a low-fat diet failed to prevent cardiovascular disease or cancer in women even when followed continuously for eight years. In women with pre-existing CVD, the low-fat diet increased the risk of CVD by 26 percent!Since the publication of the WHI results, low-fat diet supporters have been working overtime manufacturing excuses for the failure of their beloved regimen. Foremost among these is that the women in the low-fat group did not reduce their fat intake sufficiently. I even had one sadly misguided soul write to me the other day telling me I did not "understand" low-fat diets, that the only reason they frequently fail is because people following them don't lower their fat intake enough.
Such stupidity makes my head spin…
First of all, I understand low-fat diets only too well! Much to my regret, I followed one throughout most of the nineties, and the result was nothing short of disastrous.
My low-fat nightmare began in my early twenties, after a doctor told me that my cholesterol, at 213, was "moderately high" and placed me at increased risk of heart disease (something I now know to be nonsense). Following the prevailing dietary wisdom at the time, I soon adopted a low-fat diet. This wasn't your average low-fat diet--it was a VERY low-fat diet, with the kind of anemic fat intake that wouild have made lipid-phobes like Ornish and Pritikin proud.
For years, I ate only the leanest meats; in fact, to this day, the thought of eating another skinless chicken breast, kangaroo steak, or low-fat fish makes me want to puke! Fuelling the high energy demands of my daily workouts in the face of a low fat intake meant eating carbohydrates--lots of them! In keeping with the common advice still given to athletes to eat lots of 'healthy' complex carbohydrate foods, I consumed copious amounts of rye bread, brown rice, sweet potato, wholemeal pasta, rolled oats, buckwheat, and millet.
My dedication to the low-fat mantra was nothing short of religious, and my low-fat brainwashing so thorough that when I sat down and calculated the average amount of fat calories I was taking in, I was actually proud when I realized I was consistently consuming less than ten percent of my calories as fat every day!
Halfway through the nineties, reality began to bite--hard. Despite my 'healthy' diet, and my daily strenuous training regimen, my blood pressure had risen from 110/65, a reading characteristic of highly-conditioned athletes, to an elevated 130/90. I noticed it was becoming increasingly harder to maintain the lean, "ripped", vascular look that I had always prided myself on. Instead, my physique was becoming increasingly smooth and bloated. My digestive system became progressively more sluggish, my stomach often feeling heavy and distended after meals. I frequently felt tired after meals. I showed signs of leaky gut syndrome, racking up a rather impressive list of irreversible food sensitivities. I had never been much of a coffee drinker, but I was now frequently trying to fight off increasing fatigue by sipping a strong black or two before training sessions. My fasting blood glucose level was below the normal range, indicative of reactive hypoglycemia.
Basically, I felt like crap!
It wasn't until I abandoned the whole low-fat charade, and adopted a diet that went against everything preached by the reigning diet orthodoxy, that I began to reverse these symptoms. When I ate more saturated fat and meat than ever before and subsequently felt better than ever before, I quickly realized that most diet 'experts' actually had no clue what they were talking about. I quickly realized that they were mere parrots repeating an official party line.
When I look back on my fat-fearing days, where I really believed that dietary fat was some sort of heinous toxin, the first thought that comes to mind is "What a wanker!" I then think of the sad legion of brainwashed folks all around the world who still follow the idiotic low-fat paradigm. "Poor folks," I think to myself, "they really have no idea just how badly they've been had…"
While I feel sorry for many of these folks, I have nothing but utter contempt for those who write me in defense of the low-fat paradigm. To be fooled is one thing, but to vigorously defend those who have mercilessly deceived and shafted you is beyond pitiful--such self-destructive stupidity is an absolutely repugnant thing to observe!
Let's now find out why the participants in the diet group of the WHI trial should be glad that they did not lower their fat intake any more than what they did!
Why the Low-Fat Diet is a Big Fat Fraud
One of the first priorities of healthy eating is to consume the most nutrient-dense foods possible. Cutting your fat intake strongly impedes this goal via at least three mechanisms:
1) Directly slashing your intake of important vitamins and fatty acids;
2) Reducing the absorption of crucial fat-soluble vitamins;
3) Decreasing the absorption of important minerals.
You probably think you're being "enlightened" when you trim the fat from your meats and ditch your egg yolks down the sink. What you are really doing is lucidly demonstrating what a mindless, brainwashed dolt you've become. You are effectively throwing away nutrients that your body needs to survive and thrive!
The fatty portions of meat, dairy and eggs are where one finds the highest concentrations of fat-soluble vitamins such as A, D, E and beta-carotene. Stripping the skin from your chicken breast not only makes it less tasty, but reduces its vitamin A content by seventy-eight percent!(1)
Throwing away your egg yolks is equally dumb. While one large egg yolk contains 245 IU of vitamin A, 18 IU of vitamin D, and 186 mcg of lutein plus zeaxanthin, along with small amounts of other carotenoids and vitamin E, a large egg white contains none of these nutrients. Egg yolks, along with beef liver, are also an especially concentrated dietary source of phosphatidylcholine (lecithin) and choline, which the body requires for healthy liver function and for the formation of the key neurotransmitter acetylcholine. Lower levels of acetylcholine are associated with memory loss and cognitive decline(2).
The last time you chose skim milk yogurt instead of the whole milk variety, you nutritionally short-changed yourself; skim yogurt contains 93 percent less vitamin A than whole yogurt! And if you chose non-fat yogurt, then congratulations--you received no vitamin A whatsoever!(1)
Data from national nutrition surveys consistently show that American children have lower than recommended intakes of vitamin E, and this is reflected in below-average serum levels of the vitamin. Reduction in dietary fat further exacerbates the low vitamin E status of children(3). The consequences of low dietary vitamin E intakes may include impaired immune responses, and an increased susceptibility to cardiovascular disease and cancer.
Willingly reducing your consumption of important vitamins and carotenes is not smart--it's downright stupid!
Absorb This!
Low-fat eating doesn't just decrease your intake of certain crucial nutrients. As researchers have shown time and time again, it will also dramatically reduce the absorption of whatever fat-soluble vitamins and carotenes remain in your diet!(4-7).
When subjects ingested equal amounts of lutein--a carotenoid that may protect against age-related macular degeneration and cataract--from either whole eggs, spinach or supplements, it was observed that lutein absorption was significantly higher during the period of whole egg consumption(8).
In another study, researchers compared the absorption of carotenoids from salads that contained either 0, 6 or 28 grams of canola oil. There was no increase in blood carotenoid concentrations after the fat-free salad, while the reduced fat salad produced markedly lower blood carotenoid elevations than the high fat version(9).
The addition of 150 grams of fat-rich avocado to salsa enhanced lycopene and beta-carotene absorption by 4.4 and 2.6-fold, respectively, compared to avocado-free salsa. In the same subjects, adding either twenty-four grams of avocado oil or 150 grams avocado to salad greatly enhanced alpha-carotene, beta -carotene and lutein absorption by 7.2, 15.3 and 5.1 times, respectively, compared with avocado-free salad!(10)
Only a true dumbass would think that reducing absorption of healthful fat-soluble nutrients is somehow beneficial. Don't be a dumbass.
Making a Bad Situation Worse
The mineral status of the typical Westerner is atrocious. Take magnesium for example, a substance vital for healthy heart function, blood sugar control, bone formation, and muscular contraction(11-16). A recent survey of U.S. adults found that the average daily intake of magnesium among Caucasian men is only 352 milligrams, and a mere 278 milligrams among African American men. Caucasian women consume an average of 256 milligrams per day, while African American women take in only 202 milligrams daily(17). The lower amounts of magnesium ingested by African Americans have been posited as a possible contributor to their increased susceptibility of hypertension, diabetes, and cardiovascular disease(18).
The situation isn't much better for zinc. Overt zinc deficiencies are common to Third World countries where animal protein consumption is low, while milder, 'sub-clinical' zinc deficiencies appear to be common in modernized nations. Nationwide food consumption surveys by the USDA have found that the average intake of zinc for males and females of all ages is below the recommended daily allowance (RDA). This is especially worrying when one considers that RDAs are generally based on the amount of a nutrient required to prevent obvious, well-recognized deficiency diseases (such as stunted growth and hypogonadism in the case of zinc), not sub-clinical deficiencies that may damage one's health over the longer-term.
Those who follow low fat diets are at even greater risk of zinc deficiency(19,20). Not only do low-fat diets discourage the consumption of zinc-rich foods like red meat, but a low dietary fat intake itself acts to impair mineral absorption.
It's ironic that red meat is typically denigrated for its saturated fat content, because saturates are the very fats that improve mineral absorption!(21-24).
A pilot study by researchers at the USDA Grand Forks Human Nutrition Research Center examined the effect of different fats and carbohydrate on performance and mineral metabolism in three male endurance cyclists. During alternating four-week periods, each subject consumed diets in which either carbohydrate, polyunsaturated, or saturated fat contributed about fifty percent of daily energy intake. Endurance capacity decreased with the polyunsaturated fat diet. The polyunsaturated diet also resulted in increased excretion of zinc and iron, while copper retention tended to be positive only on the saturated fat diet(25).
Optimal health is next to impossible to achieve with sub-optimal mineral status. Low-fat diets, most notably those low in saturated fats, encourage sub-optimal mineral status. Yet another reason why these diets suck the salsiccia, big time!
Low-Fat, Low Omega-3
Unless you've been living on a distant planet for the last few years, then you have no doubt heard about omega-3 fats and their pivotal role in maintaining good health.
Unlike low-fat diets, clinical trials utilizing the sole intervention of increased fatty fish or fish oil intake have produced significant reductions in CHD and overall mortality. The benefits of EPA and DHA-rich items like fish and fish oil are not confined to the cardiovascular system. In epidemiological studies and animal experiments, increased intakes of long-chain omega-3 fatty acids have been associated with lower rates of cancer, depression and mental illness, adverse pregnancy outcomes, infectious disease, osteoporosis, lung disease, menstrual pain, cognitive decline in the elderly, eye damage, childhood asthma and attention-deficit hyperactivity disorder(26-51). In clinical trials with human subjects, researchers have observed benefits from long-chain omega-3 supplementation in the treatment of asthma, alzheimers, rheumatoid arthritis, depression, schizophrenia, infant health, pregnancy outcomes, kidney disease, menstrual problems, ulcerative colitis, Crohn's disease and cystic fibrosis(52-73). Hell, even the fat-hating vegetarian Dean Ornish recommends the use of distinctly non-vegetarian fish oil supplements! (Gee, can anyone see a contradiction there?)
So what has this all got to do with low-fat eating? Everything!
Similar to fat-soluble vitamins, the absorption of EPA and DHA increases when consumed with a high fat meal(74).
Again, not just any old fat will do when it comes to improving one's omega-3 status. Saturated fat improves the body's conversion of plant-source omega-3 fats into the longer-chain varieties EPA and DHA, while omega-6-rich fats impede the conversion process. In young males, elongation of alpha-linolenic acid (ALA) and linoleic acid (LA) to DHA, EPA and AA was reduced by forty to fifty percent when dietary LA intake increased from fifteen to thirty grams per day(75).
When rats were supplemented with linseed oil, their serum and tissue content of the all-important omega-3 fatty acids increased, and omega-6 levels decreased, to a far greater extent on a saturated fat-rich (beef fat) diet than on a linoleic acid-rich (safflower oil) diet(76).
Cutting fat--as in saturated fat--worsens your omega-3 status. If you think that's a good thing, then low-fat nutrition has already scrambled your brain. My advice: Eat some fat before you become totally brain dead!
Speaking of scrambled brains…
Nature's Anti-Depressant: Fat!
Feeling moody? Irritable? Always snapping at your kids for no good reason? Are you known around the office as "Attila the Grump"? If so, eating a low-fat diet isn't going to help the situation. In fact, a low-fat diet may actually be the cause of your mental funk!
In 1998, U.K. researchers reported the results of an important experiment involving twenty healthy male and female volunteers. One group was placed on a 41% fat diet, while the other group consumed a 25% fat diet. After 4 weeks had passed, the groups were swapped around so that those originally on the low-fat diet were now consuming the high-fat diet, and vice-versa. Throughout the study, all meals were prepared by the university conducting the study and supplied to the participants. Both diets were specially designed to be as palatable and similar in taste as possible.
At the beginning and end of each diet period, every subject underwent a battery of psychological assessments, including various mood state questionnaires and an interview by a psychiatrist who was blinded to the participant's dietary status.
The study was tightly-controlled and adherence to the diets appears to have been high. HDL cholesterol levels declined during the low-fat period, a typical response on low-fat, high-carb diets, indicating that subjects ate the foods as supplied.
The researchers found that, while ratings of anger-hostility slightly declined during the high-fat diet period, they significantly increased during the low-fat, high-carb diet period!
Tension-anxiety ratings declined during the high-fat period, but did not change during the four weeks of low-fat, high-carb eating.
Ratings of depression declined slightly during the high-fat period, but increased during the low-fat, high-carb period, mainly due to two of the low-fat subjects reporting significantly greater depression-dejection ratings.
What is particularly alarming about this study is that the low-fat diet produced these symptoms in mentally healthy subjects. As the researchers emphasized, the participants were "a psychologically robust group who had never previously suffered from depression or anxiety, and who were not going through any 'stressful' events during the study." They further stated that "The alterations in mood observed in the present study may have been greater if subjects were feeling more stressed or were more susceptible to mental illness."(77)
Low-fat diets should be approached with extreme caution by those with a history of depression, anxiety, overly aggressive behavior or mental illness. Such individuals may be especially vulnerable to the nutritional inadequacies of low-fat diets.
The UK researchers' observations raise some interesting questions. Could the low-fat, high-carbohydrate diets that have been so heavily promoted over the last thirty years be at least partially responsible for increases in anti-social behavior witnessed during the same period? If studies with our primate cousins are anything to go by, the answer to this question could well be affirmative.
Low-Fat Diet Makes Monkeys Go Ape
For almost 2 years, adult male monkeys were fed a "luxury" diet - (43% calories from fat, 0.34 mg cholesterol/Calorie of diet) or a "prudent" diet (30% calories from fat, 0.05 mg cholesterol/Calorie of diet).
Researchers observed that the low-fat diet monkeys were more irritable and initiated more aggression than the "luxury" diet animals.
The prudent diet resulted in lower total serum cholesterol levels, something that our absent-minded health authorities automatically assume is a good thing. The researchers, however, noted: "These results are consistent with studies linking relatively low serum cholesterol concentrations to violent or antisocial behavior in psychiatric and criminal populations and could be relevant to understanding the significant increase in violence-related mortality observed among people assigned to cholesterol-lowering treatment in clinical trials."(78)
Fatless Shrugged
It was Ayn Rand who once said that the most noble and productive goal for a person to engage in was the pursuit of their own happiness. If the achievement of your own happiness is important to you, then kick the low-fat diet's sad, sorry, melancholy butt right out of your life--it's a loser. Low-Fat Diets Lower Testosterone
Testosterone is abhorred by politically correct weenies, who like to blame it for every instance of disagreeable male behavior, in much the same way menstruation was once cited as the catch-all explanation for uncharacteristically aggressive or irritable female behavior.
Of course, scientific reality is of little concern to the politically correct. The fact is, testosterone is an extremely important hormone for both men and women. Sex drive, muscle and bone health, immune function, cognitive function, mood, and cardiovascular health are all negatively affected by declining levels of testosterone. Testosterone levels typically decline with age, and, along with the decline of other key hormones, falling T levels are believed to be a major contributor to many of the deleterious changes seen during the aging process. As such, aging individuals should be looking at ways to preserve and even boost their testosterone status, rather than engaging in self-defeating habits that will speed the decline in T levels. Alcohol abuse, recreational drug use, pharmaceutical drugs, stress, and poor sleep habits can all lower testosterone levels.
So too can low-fat diets.
Research shows that reducing fat intake from around forty percent to 20-25 percent of calories decreases testosterone output. Low fat diets also increase levels of sex hormone-binding globulin (SHBG), a protein which binds to testosterone, thus reducing the amount of bioavailable, or 'free', testosterone in the body. It is free testosterone that is responsible for this hormone's favorable effects on growth, repair, sexual capacity and immune function(79-81).
Again, not just any old fat will suffice when it comes to optimizing testosterone levels. A study with weight-training men showed higher saturated fat and monounsaturated fat consumption to be positively associated with testosterone levels. In contrast, higher dietary levels of so-called "heart-healthy" polyunsaturated fats relative to saturated fats were associated with lower testosterone levels (82).
It's highly ironic that athletes and bodybuilders will take all manner of expensive, esoteric and often dubious testosterone-boosting concoctions--not to mention anabolic steroids--yet will follow hormone-damping low-fat diets with religious fervor. It's a little like putting on a weighted vest before a big race and expecting to run at full speed.
Hormones like testosterone play a fundamentally important role in stimulating and regulating growth and metabolism. Don't go throwing a low-fat monkey wrench into your metabolic engine!
Low-Fat Diets and Immune FunctionDiet 'experts' assure us that a low-fat diet is the key to good health. The published research does not support such claims.
Despite the virulent ranting of anti-fat activists, trials comparing sedentary adult volunteers fed low-fat diets with those receiving higher fat diets has shown no improvement in immune status in the former group(83,84).
In children, whole milk consumption is associated with fewer gastrointestinal infections than consumption of low fat milk (85). Rats consuming diets high in milk fat show a significantly greater resistance to Listeria infection and higher survival rates than those whose diets were low in milk fat(86). Similar results have been observed in mice fed diets high in saturate-rich coconut oil(87)
In athletes, who are constantly pushing their immune systems to the edge with strenuous training, adherence to the commonly-recommended low-fat high-carbohydrate diet (15-19% of total calories) increases pro-inflammatory immune factors, decreases anti-inflammatory factors, and depresses antioxidant status when compared to higher fat diets (30-50% of total calories)(88,89). Such changes may leave athletes on low-fat diets with a lowered resistance to infection and a higher risk of chronic illness. This may be due to difficulty in obtaining sufficient calories from low-fat diets to meet the energy demands of exercise; increasing dietary fat intake and total caloric intake to match energy expenditure appears to reverse the negative effects on immune function reported on calorie-deficient, low-fat diets. Diets comprising 32% to 55% fat also improve endurance capacity compared to diets with 15% fat(90).
It was Scandinavian researchers who, in the 1960s, performed research showing that using extremely high-carbohydrate, low-fat diets for short periods could enhance athletic performance. This was achieved by using these diets as part of a "depletion-repletion" carbohydrate-loading strategy, which helped temporarily elevate muscle glycogen stores to higher than usual levels. One of the pioneers in this area, Dr. Jan Karlsson, points out that such diets were never intended to be applied for more than 3-4 days. Karlsson and his colleagues openly lament that these diets are now employed for extended periods of time, and refer to the prolonged use of very high-carbohydrate/low-fat diets by athletes as "voluntary malnourishment". They note that in Scandinavia, researchers use the term "Carbohydrate Trap" when referring to the widespread belief that these diets are required for optimal performance. These researchers consider a 50-55% carbohydrate, 35% fat diet to be eminently more sensible and nutritious than the >60% carb, <25% fat diets commonly used by athletes(91).
For athletes and non-athletes alike, the low-fat diet is a sick (pun intended) joke.
The Low-Fat Diet Does Not Protect Against Heart Disease, and May Actually Worsen It
The WHI trial confirmed what well-read cholesterol skeptics have known for a long time: The low-fat diet is a big fat fraud when it comes to preventing heart disease. Among the 48,835 women participating in the trial, no significant differences in CHD or stroke incidence, CHD or stroke mortality, or total mortality were observed(92). Nor were there any reductions in the incidence or mortality rates of breast cancer, colorectal cancer, or total cancer(93,94).
There was however, one very ominous finding to emerge from the WHI trial. Among the 3.4 percent of trial participants with pre-existing cardiovascular disease, those randomized to the low-fat diet experienced a 26% increase in the relative risk of non-fatal and fatal CHD!
Low-fat advocates have remained deafeningly silent on this inconvenient finding, and would no doubt like to believe this was just a 'freak' occurrence. However, this is hardly the first time that low-fat eating has been shown to worsen the prognosis of women with existing cardiovascular disease.
In 2004, the world's most prominent nutrition journal, The American Journal of Clinical Nutrition, published the results of a very, very interesting study. Harvard researchers had taken 235 postmenopausal women with established coronary heart disease, and divided them into four categories according to their level of saturated fat intake. They then performed coronary angiographies at baseline and after a mean follow-up of 3.1 years, analyzing over 2,200 coronary artery segments in the process.
After adjusting for multiple confounders, a higher saturated fat intake was associated with less narrowing of the arteries and less progression of coronary atherosclerosis. Compared with a 0.22 mm narrowing in the lowest quartile of intake, there was a 0.10-mm narrowing in the second quartile, a 0.07 mm narrowing in the third quartile, and no narrowing in the fourth and highest quartile of saturated fat intake!
Following a low-fat diet means adopting a high-carbohydrate diet by default. After all, it is exceedingly difficult and highly unpalatable to achieve the bulk of one's caloric needs by eating lean protein foods. It is of no small concern then, that carbohydrate intake was positively associated with atherosclerotic progression, particularly when the glycemic index was high. The intake of so-called 'heart-healthy' polyunsaturated fats was also positively associated with progression of atherosclerosis, but monounsaturated and total fat intakes were not associated with progression (it must be noted that the major sources of polyunsaturates in Western countries are refined vegetable oils which are rich in the omega-6 fat linoleic acid. The polyunsaturated omega-3 fats, which are underconsumed by most Westerners, have actually been shown to lower CVD).
After examining the baseline data for the study subjects, it is apparent that the results can not be explained away by otherwise healthier lifestyles among those eating the most saturated fat; the high saturated fat group, in fact, had the greatest number of current smokers! Women eating the most saturated fat were also less likely to take blood-thinning medications like aspirin(95).
If this study had found saturated fats to be associated with cardiovascular disease, its results would have been trumpeted in headlines around the world. Instead, they were largely ignored by the mainstream media and our ever-so responsible 'health' authorities. It appears only studies that support the cherished dogma of our health orthodoxy are considered suitable as press release fodder…
A major factor in the progression of cardiovascular disease--and most major diseases--is free radical damage. It is well-established that saturated fatty acids, because of their lack of vulnerable double bonds, are the least susceptible to free radical damage; polyunsaturates are the most vulnerable. We also know that increased carbohydrate consumption, especially of the refined variety, does an outstanding job of raising blood sugar and insulin levels, which accelerates glycation, free radical activity, blood clot formation, and arterial smooth muscle cell proliferation.
It should also be noted that increasing heart disease incidence throughout the twentieth century has been accompanied by increasing polyunsaturate consumption, while a marked increase in refined carbohydrate consumption during the last three decades has been accompanied by spiralling obesity and diabetes incidence. Animal fat consumption, in contrast, has remained stable over the last 100 years.
So what we have is two studies that show that women with pre-existing heart disease will experience WORSE outcomes if they shun saturated fat and opt for a low-fat/high-carbohydrate diet! Furthermore, the validity of these results is supported by basic biochemistry and epidemiological data. So will low-fat advocates stop recommending this pattern of eating to women with heart disease? Does their concern for human life override their need to defend their precious low-fat dogma at all costs?
I truly doubt it…
If low-fat advocates won't be straight with you, then I will. Let's be perfectly clear on this: If you are female, and suffer cardiovascular disease, the published, peer-reviewed scientific evidence indicates that adopting a low-fat diet could be DEADLY.
The WHI is not the only dietary intervention trial to demonstrate the worthlessness of the low-fat diet in preventing CVD. In 1965, the prominent journal Lancet published the results of a trial conducted by the UK Medical Research Committee. In this study, 264 men under 65 were assigned to either a low-fat diet or their usual diet. Dietary records show that those in the low-fat group averaged 45 g/day of fat throughout the trial, while those in the control group actually increased their average fat intake from 106 to 125g. The average serum cholesterol measurement of the low-fat group was 25 points lower than that of the control group at 4 years. Despite nonsensical claims that "every 1mg'dl drop in cholesterol equals a 2% drop in CHD risk", there were no differences between the two groups in CHD incidence or mortality after 4 years.
In Search of the Elusive 'Negative Fat Intake'!
The hysterical anti-fat vitriole that spews forth from some anti-fat faddists leads me to believe that if these clowns could eat a 'negative-fat' diet, they would! As for their argument that the above trials didn't lower fat enough, one has to wonder how creating even greater deficiencies in valuable nutrients, and predisposing one to greater risk of depression and anger--all of which low-fat diets have indeed been clinically documented to do--will in any way help prevent heart disease! Maybe these folks have been eating low-fat so long that it's started to drain their brains; healthy human brains, after all, are 60% fat by weight!
The authors of the MRC trial concluded that: "A low-fat diet has no place in the treatment of myocardial infarction." Despite being written over forty years ago, these words have largely been ignored by a medical and health hierarchy which seems to earnestly believe that if only it keeps flogging the dead low-fat horse, it will one-day magically spring to life. In Australia, this is known as engaging in a 'wank', which means that people who push low-fat diets despite no proof whatsoever of their efficacy are wankers. This might be stating the obvious, but…you really shouldn't listen to wankers!
But the Japanese Eat a Low-Fat Diet…Don't They?
Supporters of low-fat nutrition cite the Japanese ad nauseum, claiming that their low-fat/high-carbohydrate diet is the reason for their low rate of heart disease. It is ironic that many of these same commentators exhort the benefits of whole-grains and tell us that the only 'bad' carbohydrates are those that come from refined sugars and grains. These folks need to get their story straight---a major source of carbohydrates in the Japanese diet is white rice--a refined grain! That means that if the high-carbohydrate Japanese diet is cardio-protective, then refined grains must be good for one's heart! Well, which is it? You can have it both ways; either refined grains are heart-friendly, or they're not!
The truth is, the longevity and low CHD incidence of the Japanese owes nothing to carbohydrate intake, refined or otherwise. During the 1960s and 1970s, industrialization underwent rapid growth in Japan. This period of marked economic change bought with it greater consumption of animal protein and fat. This increased animal food consumption in Japan has been accompanied by a marked decline in both the overall incidence of and the mortality from one of that nation's biggest killers--stroke. This increase in animal protein and animal fat consumption has also occurred alongside Japan's rise to the top of the longevity ladder.(96,97)
If you're tempted to write this off as merely a consequence of improved living standards and medical technology, keep in mind that long-term follow-up studies with both native and migrant Japanese populations show that those who eat the most animal protein and animal fat enjoy greater longevity and a lower incidence of stroke than those who eat lesser amounts(98-101).
OK, So What About the Mediterranean Diet?
A diet low in saturated fat is purportedly a major factor in the low rates of CHD observed in Southern European countries. Just one wee problem: France, the Mediterranean country with the lowest CHD rates of all, is also the Mediterranean country with the highest saturated fat intake!
Oops!
Health 'experts' have tried to brush off this embarrassing observation as a 'paradox' (orthodoxy loves applying the 'paradox' label to uncomfortable contradictions) by claiming that red wine explains this difference. If that were true, then the Italians, who drink a similar amount of red wine, should have CHD rates even lower than France. But they don't; their CHD rates are similar to those of other Southern European countries where far less red wine is consumed(102).
Conclusion
I could go on, and on, and on…but I'll just close by saying that the low-fat diet has NEVER been demonstrated to do all the wonderful health-fortifying things claimed for it. The only trials showing favorable effects in people following low-fat diets are those that simultaneously employed other truly useful interventions, like exercise, stress management, increased fruit and vegetable intake and decreased processed food intake, and weight loss. However, there is absolutely no law whatsoever stating that low-fat eating is required for the implementation of any of these strategies. In fact, given the available evidence, one can only conclude that the inclusion of higher fat intakes in these trials may even have improved the results!
The bottom line: Not only is low-fat eating a boring way to go through life, it is a useless and often counterproductive hoax.
References and Assorted Disclaimers:
DISGRUNTLED WORSHIPPERS OF THE LOW-FAT RELIGION SHOULD READ THE FOLLOWING:I have not stated anything in this article that cannot be verified by published, peer-reviewed research. Nonetheless, my inbox will no doubt be flooded with angry emails from those who have been brainwashed by the low-fat paradigm, and who violently object to the thought that something that they have believed in so strongly for so long might actually be false. In other words, malevolent dimwits who want to shoot the messenger! For those of you who fall into this category, my suggestions are as follows: 1) GROW UP!; 2) Start placing a premium on discovering the facts, as opposed to doggedly defending what you have already decided you want to believe; 3) Instead of attacking me, start questioning the motives of those who profit greatly from the fallacious anti-fat, anti-cholesterol paradigm. This includes the food and drug conglomerates that make BILLIONS from the sale of low-fat foods and cholesterol-lowering drugs, the health and dietetic 'associations/organizations/institutes/foundations/etc' who receive millions in 'donations' from these very same companies, and the executives of these so-called 'non-profit' organizations who enjoy six-figure incomes and extensive perquisites.
To attack the owner of a non-commercial web site, who has nothing to gain financially by either supporting or opposing the low-fat paradigm, and defending those WHO DO, is so bloody stupid that it defies comprehension. Unfortunately, there are a lot of bloody stupid people in the world! If you are one of them, and decide to write me, please note that unless your email contains valid references to the scientific literature, it will be deleted immediately. After having established yourself as an ignorant goofball, your email address will also be added to my spam filter and any further emails will be delivered straight to my trash. Sorry, but I really am extremely busy and have no time or patience for ignorant, time-wasting twits.
NOTE: I have no problem with people reprinting this article on other web sites for non-commercial purposes. Heck, you can post it on the side of the Empire State Building for all I care (just be sure to seek permission from the owners first). However, PLEASE ENSURE that you give full credit to the author, whether you reproduce the article in whole or part. A hyperlink to www.TheOmnivore.com would also be greatly appreciated! Those wishing to reprint this or any other article on TheOmnivore.com for commercial purposes should email: ac.theomnivore@gmail.com
References
1. USDA National Nutrient Database for Standard Reference. Available online: http://www.nal.usda.gov/fnic/foodcomp/search/
2. Giacobini E. Cholinergic function and Alzheimer's disease. Int J Geriatr Psychiatry. 2003 Sep; 18 (Suppl 1): S1-S5.
3. Bendich A. Vitamin E status of US children. Journal of the American College of Nutrition, Aug, 1992; 11 (4): 441-444.
4. Takyi EE. Children's consumption of dark green, leafy vegetables with added fat enhances serum retinol. Journal of Nutrition, 1999; 129 (8): 1549-1554.
5. Jalal F, et al. Serum retinol concentrations are affected by food sources of ß-carotene, fat intake, and anthehelmintic drug treatment. American Journal of Clinical Nutrition, 1998; 68: 623-629.
6. Roodenburg JA, et al. Amount of fat in the diet affects bioavailability of lutein esters but not of {alpha}-carotene, {beta}-carotene, and vitamin E in humans. American Journal of Clinical Nutrition, 2000; 71 (5): 1187-1193.
7. Drammeh BS, et al. A Randomized, 4-Month Mango and Fat Supplementation Trial Improved Vitamin A Status among Young Gambian Children. Journal of Nutrition, 2002; 132 (12): 3693 - 3699.
8. Chung H-Y, et al. Lutein Bioavailability Is Higher from Lutein-Enriched Eggs than from Supplements and Spinach in Men. Journal of Nutrition, 2004; 134: 1887-1893.
9. Brown MJ, et al. Carotenoid bioavailability is higher from salads ingested with full-fat than with fat-reduced salad dressings as measured with electrochemical detection. American Journal of Clinical Nutrition, Aug. 2004; 80: 396-403.
10. Unlu NZ, et al. Carotenoid Absorption from Salad and Salsa by Humans Is Enhanced by the Addition of Avocado or Avocado Oil. Journal of Nutrition, Mar, 2005; 135: 431-436.
11. Fox C, et al. Magnesium: its proven and potential clinical significance. Southern Medical Journal, Dec, 2001; 94 (12): 1195-1201.
12. Shechter M, et al. Effects of oral magnesium therapy on exercise tolerance, exercise-induced chest pain, and quality of life in patients with coronary artery disease. American Journal of Cardiology, Mar 1, 2003; 91 (5): 517-521.
13. Shechter M, et al. Beneficial antithrombotic effects of the association of pharmacological oral magnesium therapy with aspirin in coronary heart disease patients. Magnesium Research, Dec, 2000; 13 (4): 275-284.
14. Shechter M, et al. Oral magnesium therapy improves endothelial function in patients with coronary artery disease. Circulation, Nov 7, 2000; 102 (19): 2353-2358.
15. Guerrero-Romero F, et al. Oral magnesium supplementation improves insulin sensitivity in non-diabetic subjects with insulin resistance. A double-blind placebo-controlled randomized trial. Diabetes & Metabolism, Jun, 2004; 30 (3): 253-258.
16. Rodriguez-Moran M, Guerrero-Romero F. Oral magnesium supplementation improves insulin sensitivity and metabolic control in type 2 diabetic subjects: a randomized double-blind controlled trial. Diabetes Care, Apr, 2003; 26 (4): 1147-1152.
17. Ford ES, Mokdad, AH. Dietary Magnesium Intake in a National Sample of U.S. Adults. Journal of Nutrition, 2003; 133: 2879-2882.
18. Fox CH, et al. Magnesium deficiency in African-Americans: does it contribute to increased cardiovascular risk factors? Journal of the National Medical Association, 2003 Apr; 95 (4): 257-62.
19. Retzlaff BM, et al. Changes in vitamin and mineral intakes and serum concentrations among free-living men on cholesterol-lowering diets: the Dietary Alternatives Study. American Journal of Clinical Nutrition, 1991; 53 (4): 890-898.
20. Baghurst KI, et al. Demographic and dietary profiles of high and low fat consumers in Australia. Journal of Epidemiology and Community Health, 1994; 48 (1): 26-32.
21. Mahoney AW, et al. Effects of level and source of dietary fat on the bioavailability of iron from turkey meat for the anemic rat. Journal of Nutrition, 1980: 110 (8): 1703-1708.
22. Johnson PE, et al. The effects of stearic acid and beef tallow on iron utilization by the rat. Proc Soc Exp Biol Med, 1992; 200 (4): 480-486.
23. Koo SI, Ramlet JS. Effect of dietary linoleic acid on the tissue levels of zinc and copper, and serum high-density lipoprotein cholesterol. Atherosclerosis, 1984; 50 (2): 123-132.
24. Van Dokkum W, et al. Effect of variations in fat and linoleic acid intake on the calcium, magnesium and iron balance of young men. Ann Nutr Metab, 1983; 27 (5): 361-369.
25. Lukaski HC, et al. Interactions among dietary fat, mineral status, and performance of endurance athletes: a case study. Int J Sport Nutr Exerc Metab, Jun 2001; 11 (2): 186-198.
26. Ip, et al. Requirement of essential fatty acid for mammary tumorigenesis in the rat. Cancer Research, 1985; 45 (5): 1997-2001.
27. Rose DP. Effects of dietary fatty acids on breast and prostate cancers: evidence from in vitro experiments and animal studies. American Journal of Clinical Nutrition, Dec, 1997; 66 (6 Suppl): 1513S-1522S.
28. Fernandez E, et al. Fish consumption and cancer risk. American Journal of Clinical Nutrition, Jul 1, 1999; 70(1): 85-90.
29. Terry P, et al. Fatty fish consumption and risk of prostate cancer. Lancet, Jun 2, 2001; 357 (9270): 1764-1766.
30. Terry P, et al. Fatty fish consumption lowers the risk of endometrial cancer: a nationwide case-control study in Sweden. Cancer Epidemiology, Biomarkers & Prevention, Jan, 2002; 11 (1): 143-145.
31. Maillard V, et al. N-3 and N-6 fatty acids in breast adipose tissue and relative risk of breast cancer in a case-control study in Tours, France. International Journal of Cancer, Mar 1, 2002; 98 (1): 78-83.
32. Kato I, et al. Prospective study of diet and female colorectal cancer: the New York University Women's Health Study. Nutrition and Cancer, 1997; 28: 276-281.
33. Hakim IA, et al. Fat intake and risk of squamous cell carcinoma of the skin. Nutrition and Cancer, 2000; 36 (2): 155-162.
34. Tanskanen A, et al. Fish Consumption and Depressive Symptoms in the General Population in Finland. Psychiatric Services, Apr, 2001; 52: 529-531.
35. Adams PB, et al. Arachidonic acid to eicosapentaenoic acid ratio in blood correlates positively with clinical symptoms of depression. Lipids, Mar, 1996; 31 (Suppl): S157-161.
36. Mamalakis G, et al. Depression and adipose essential polyunsaturated fatty acids. Prostaglandins, Leukotrienes, and Essential Fatty Acids, Nov, 2002; 67 (5): 311-318.
37. Laugharne JD, et al. Fatty acids and schizophrenia. Lipids, Mar, 1996; 31 (Suppl): S163-165.
38. Olsen SF, Secher NJ. Low consumption of seafood in early pregnancy as a risk factor for preterm delivery: prospective cohort study. British Medical Journal, Feb 23, 2002; 324: 447.
39. Williams MA, et al. Omega-3 fatty acids in maternal erythrocytes and risk of preeclampsia. Epidemiology, May, 1995; 6 (3): 232-237.
40. Hibbeln JR. Seafood consumption, the DHA content of mothers' milk and prevalence rates of postpartum depression: a cross-national, ecological analysis. Journal of Affective Disorders, May, 2002; 69(1-3): 15-29.
41. Turek JJ, et al. Dietary polyunsaturated fatty acids modulate responses of pigs to Mycoplasma hyopneumoniae infection. Journal of Nutrition, Jun, 1996; 126 (6): 1541-1548.
42. Tully AM, et al. Low serum cholesteryl ester-docosahexaenoic acid levels in Alzheimer's disease: a case-control study. British Journal of Nutrition, Apr, 2003; 89 (4): 483-489.
43. Requirand P, et al. Serum fatty acid imbalance in bone loss: example with periodontal disease. Clinical Nutrition, Aug, 2000; 19 (4): 271-276.
44. Watkins BA, et al. Nutraceutical Fatty Acids as Biochemical and Molecular Modulators of Skeletal Biology. Journal of the American College of Nutrition, 2001; 20 (90005): 410S-416S.
45. Reinwald S, et al. Repletion with (n-3) Fatty Acids Reverses Bone Structural Deficits in (n-3)-Deficient Rats. Journal of Nutrition, Feb 2004; 134: 388-394.
46. Schwartz J. Role of polyunsaturated fatty acids in lung disease. American Journal of Clinical Nutrition, Jan 2000; 71 (suppl): 393S-96S.
47. Shahar E, et al. Dietary n-3 polyunsaturated fatty acids and smoking-related chronic obstructive pulmonary disease. New England Journal of Medicine, Jul 28, 1994: 331 (4): 228-233.
48. Deutch B. Menstrual pain in Danish women correlated with low n-3 polyunsaturated fatty acid intake. European Journal of Clinical Nutrition, 1995; 49: 508-516.
49. Kalmijn, S., et al. Polyunsaturated fatty acids, antioxidants, and cognitive function in very old men. American Journal of Epidemiology, Jan 1, 1997: 145: 33-41.
50. Seddon JM, et al. Dietary Fat and Risk for Advanced Age-Related Macular Degeneration. Archives of Ophthalmology, 2001; 119 (8): 1191-1199.
51. Hodge L, et al. Consumption of oily fish and childhood asthma risk. Medical Journal of Australia, 1996; 164: 137-140.
52. Dry J, Vincent D. Effect of a fish oil diet on asthma: results of a 1-year double-blind study. International Archives of Allergy and Applied Immunology, 1991; 95 (2/3): 156-157.
53. Burgess JR, et al. Long-chain polyunsaturated fatty acids in children with attention-deficit hyperactivity disorder. American Journal of Clinical Nutrition, 2000; 71: 327-330.
54. Yehuda S, et al. Essential fatty acids preparation (SR-3) improves Alzheimer's patients quality of life. International Journal of Neuroscience, Nov, 1996; 87 (3-4): 141-149.
55. Geusens P et al. Long-term effect of omega-3 fatty acid supplementation in active rheumatoid arthritis, a 12-month, double-blind, controlled study. Arthritis & Rheumatism, Jun, 1994; 37 (6): 824-829.
56. Schiz Peet M, Horrobin DF. A dose-ranging study of the effects of ethyl-eicosapentaenoate in patients with ongoing depression despite apparently adequate treatment with standard drugs. Archives of General Psychiatry, Oct, 2002; 59 (10): 913-919.
57. Stoll AL, et al. Omega 3 fatty acids in bipolar disorder: a preliminary double-blind, placebo-controlled trial. Archives of General Psychiatry, May, 1999; 56 (5): 407-412.
58. Peet M, et al. Two double-blind placebo-controlled pilot studies of eicosapentaenoic acid in the treatment of schizophrenia. Schizophrenia Research, Apr 30, 2001; 49 (3): 243-251.
59. Peet M, Horrobin DF. A dose-ranging exploratory study of the effects of ethyl-eicosapentaenoate in patients with persistent schizophrenic symptoms. Journal of Psychiatric Research, Jan-Feb, 2002; 36 (1): 7-18.
60. Hamazaki T, et al. The Effect of Docosahexaenoic Acid on Aggression in Young Adults. A Placebo-controlled Double-blind Study. Journal of Clinical Investigation, Feb, 1996; 97 (4): 1129-1134.
61. Jorgensen MH, et al. Effect of formula supplemented with docosahexaenoic acid and gamma-linolenic acid on fatty acid status and visual acuity in term infants. Journal of Pediatric Gastroenterology and Nutrition, 1998; 26: 412-421.
62. Carlson SE, et al. Visual acuity and fatty acid status of term infants fed human milk and formulas with and without docosahexaenoate and arachidonate from egg yolk lecithin. Pediatric Research, 1996; 39: 882-888.
63. O'Connor DL, et al. Growth and Development in Preterm Infants Fed Long-Chain Polyunsaturated Fatty Acids: A Prospective, Randomized Controlled Trial. Pediatrics, Aug 1, 2001; 108 (2): 359-371.
64. Helland IB, et al. Maternal Supplementation With Very-Long-Chain n-3 Fatty Acids During Pregnancy and Lactation Augments Children's IQ at 4 Years of Age. Pediatrics, Jan, 2003; 111 (1): e39-e44.
65. Dunstan JA, et al. Fish oil supplementation in pregnancy modifies neonatal allergen-specific immune responses and clinical outcomes in infants at high risk of atopy: a randomized, controlled trial. Journal of Allergy and Clinical Immunology, Dec, 2003; 112 (6): 1178-1184.
66. Olsen SF, et al. Randomised controlled trial of effect of fish-oil supplementation on pregnancy duration. Lancet, Apr 25, 1992; 339 (8800): 1003-1007.
67. Olsen SF, Secher NJ. A possible preventive effect of low-dose fish oil on early delivery and pre-eclampsia: indications from a 50-year-old controlled trial. British Journal of Nutrition, Nov, 1990; 64 (3): 599-609.
68. De Caterina R et al. n-3 fatty acids and renal diseases. American Journal of Kidney Diseases, Sept, 1994; 24 (3): 397-415.
69. Harel Z et al. Supplementation with omega-3 polyunsaturated fatty acids in the management of dysmenorrhea in adolescents. American Journal of Obstetrics & Gynecology, Apr, 1996; 174 (4): 1335-1338.
70. Aslan A, Triadafilopoulos G. Fish oil fatty acid supplementation in active ulcerative colitis: A double-blind, placebo-controlled, crossover study. American Journal of Gastroenterology, Apr, 1992; 87: 432-37.
71. Salomon, P., et al. Treatment of ulcerative colitis with fish oil n-3 omega fatty acid: an open trial. Journal of Clinical Gastroenterology, Apr, 1990; (12): 157-1161.
72. Belluzzi A et al. Effect of an enteric-coated fish-oil preparation on relapses in Crohn's disease. New England Journal of Medicine, Jun 13, 1996; 334 (24): 1557-1560.
73. Lawrence R, Sorrell T. Eicosapentaenoic acid in cystic fibrosis: evidence of a pathogenetic role for leukotriene B4. Lancet, Aug 21, 1993; 342: 465-469.
74. Lawson LD, Hughes BG. Absorption of eicosapentaenoic acid and docosahexaenoic acid from fish oil triacylglycerols or fish oil ethyl esters co-ingested with a high-fat meal. Biochem Biophys Res Commun, Oct 31, 1988; 156 (2): 960-963.
75. Emken EA, et al. Dietary linoleic acid influences desaturation and acylation of deuterium-labeled linoleic and linolenic acids in young adult males. Biochim Biophys Acta, Aug 4, 1994; 1213 (3): 277-288.
76. Garg ML, et al. Dietary saturated fat level alters the competition between alpha-linolenic and linoleic acid. Lipids 1989 Apr;24(4): 334-339.
77. Wells AS, et al. Alterations in mood after changing to a low-fat diet. British Journal of Nutrition, Jan, 1998; 79 (1): 23-30.
78. Kaplan JR, et al. The effects of fat and cholesterol on social behavior in monkeys. Psychosom Med. 1991 Nov-Dec; 53 (6): 634-642.
79. Hamalainen EK, et al. Decrease of serum total and free testosterone during a low-fat high-fibre diet. J Steroid Biochem. Mar 1983; 18 (3): 369-370.
80. Reed MJ, et al. Dietary lipids: an additional regulator of plasma levels of sex hormone binding globulin. J. Clin. Endocrinol. Metab, 1987; 64: 1083-1085.
81. Dorgan JF, et al. Effects of dietary fat and fiber on plasma and urine androgens and estrogens in men: a controlled feeding study. Am J Clin Nutr. Dec 1996; 64 (6): 850-855.
82. Volek JS, et al. Testosterone and cortisol in relationship to dietary nutrients and resistance exercise. Journal of Applied Physiology, Jan 1997; 82 (1): 49-54.
83. Kelley DS, et al. Energy restriction decreases number of circulating natural killer cells and serum levels of immunoglobulins in overweight women. European Journal of Clinical Nutrition, Jan, 1994; 48 (1): 9-18.
84. van het Hof KH, et al. A long-term study on the effect of spontaneous consumption of reduced fat products as part of a normal diet on indicators of health. International Journal of Food Sciences and Nutrition, Jan, 1997; 48 (1): 19-29.
85. Koopman JS, et al. Milk fat and gastrointestinal illness. Am. J. Public Health 1984; 74: 1371-1373
86. Puertollano MA, et al. Relevance of Dietary Lipids as Modulators of Immune Functions in Cells Infected with Listeria monocytogenes. Clinical and Diagnostic Laboratory Immunology, Mar. 2002; 9 (2): 352-357.
87. de Pablo MA, et al. Determination of natural resistance of mice fed dietary lipids to experimental infection induced by Listeria monocytogenes. FEMS Immunol Med Microbiol. 2000 Feb;27(2):127-33.
88. Meksawan K, et al. Effect of dietary fat intake and exercise on inflammatory mediators of the immune system in sedentary men and women. Journal of the American College of Nutrition, Aug, 2004; 23 (4): 331-340.
89. Venkatraman JT, et al. Dietary fats and immune status in athletes: clinical implications. Medicine and Science in Sports and Exercise, Jul, 2000; 32 (7 Suppl): S389-S395.
90. Pendergast DR, et al. A perspective on fat intake in athletes. Journal of the American College of Nutrition, 2000 Jun; 19 (3): 345-350.
91. Göransson U, et al. The 'Are´ Sport Nutratherapy Program: The Rationale for Food Supplements in Sports Medicine. In: Simopoulos AP, Pavlou KN (eds). Nutrition and Fitness: Metabolic and Behavioral Aspects in Health and Disease. World Review of Nutrition and Dietetics, 1997; 82: 101-121.
92. Howard BV, et al. Low-Fat Dietary Pattern and Risk of Cardiovascular Disease: The Women's Health Initiative Randomized Controlled Dietary Modification Trial. Journal of the American Medical Association, Feb 8, 2006; 295: 655-666.
93. Prentice RL, et al. Low-Fat Dietary Pattern and Risk of Invasive Breast Cancer: The Women's Health Initiative Randomized Controlled Dietary Modification Trial. Journal of the American Medical Association, Feb 8, 2006; 295: 629-642.
94. Beresford SAA, et al. Low-Fat Dietary Pattern and Risk of Colorectal Cancer: The Women's Health Initiative Randomized Controlled Dietary Modification Trial. Journal of the American Medical Association, Feb 8, 2006; 295: 643-654.
95. Mozaffarian D, et al. Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. American Journal of Clinical Nutrition, 2004; 80: 1175-1184.
96. Tanaka H, et al. Secular trends in mortality for cerebrovascular disease in Japan, 1960-1979. Stroke, 1982; 13: 574-581.
97. Nakayama C, et al. A 15.5-Year Follow-up Study of Stroke in a Japanese Provincial City: The Shibata Study. Stroke, Jan 1, 1997; 28(1): 45-52.
98. Iso H, et al. Fat and protein intakes and risk of intraparenchymal hemorrhage among middle-aged Japanese. American Journal of Epidemiology, Jan 1, 2003; 157 (1): 32-39.
99. Abbott RD, et al. Effect of dietary calcium and milk consumption on risk of thromboembolic stroke in older middle-aged men: The Honolulu Heart Program. Stroke, May 1996; 27: 813 - 818.
100. Sauvaget C, et al. Intake of animal products and stroke mortality in the Hiroshima/Nagasaki Life Span Study. International Journal of Epidemiology, Aug 1, 2003; 32 (4): 536-543.
101. Sauvaget C, et al. Animal Protein, Animal Fat, and Cholesterol Intakes and Risk of Cerebral Infarction Mortality in the Adult Health Study. Stroke, 2004; 35: 1531.
102. Food intake data from Food and Agriculture Organization of the United Nations, Statistical Database. CHD mortality data from World Health Statistics Annual, 1961, 1966 and 1997-1999 editions.
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